There is a strange pressure to always be productive and useful.

Another email answered.

Another meal on the table.

Another person looked after.

Another day of holding it all together.

For most of us it may look much the same, or different: the job, the family, perhaps loved ones who need more of you now, a list that refills itself overnight.

Somewhere along the way, being dependable brings the danger of never stopping.

But nature doesn’t work like that.

The tide comes in. The tide goes out.

The seasons change.

Fields are left fallow so that they can become fertile again.

And the heart, the organ at the centre of this publication, spends more of its life resting than working. I find this remarkable: the heart muscle receives its own blood supply mainly between beats. While it contracts, the vessels running through it are squeezed shut. Only in the pause do the coronary arteries fill. A heart that never rested would starve.

So for the next two weeks, I’m going to follow the body’s physiology. I’m leaving for my summer holiday, and I’m going to rest.

I have a long list of things I plan to write for you. I’d like to come back to it with fresh eyes and renewed energy.

If you’ve been working through the programme, or have started rebuilding your health the same principle applies to you.

Muscle is built in the days between training sessions.

Deep sleep is when growth hormone is released and tissue is repaired.

Rest is when the rebuilding happens. So consider these two weeks part of the process, the same as the rest day in a training plan.

Let what you’ve already changed settle in.

Read those articles you’ve missed or planned to go back to.

And I hope you’ll take a little time for yourself as I will.

Read something that has nothing to do with work.

Watch a sunrise.

Watch a sunset.

Take a long, unhurried walk.

Sit by the sea if you’re lucky enough to be near one.

Or just allow yourself an afternoon with nowhere to be.

One more thing before my leave

There will be no articles in your inbox for two weeks.

But for the readers who use the Substack app, I’m not going anywhere.

Between articles, I post precious Notes: short pieces, a few sentences at a time. An important study finding too interesting to ignore. A reader’s question that deserves a public answer. Something from practice that made me stop and think. I’ll keep posting them right through my holiday. These are intended to keep you going.

Here is the thing about Notes: they never arrive to you by email. If you read me only in your inbox, you have never seen a single one, and for the next two weeks you would hear nothing from me at all. The readers in the app, meanwhile, will hear from me every day through the app.

If you’ve been meaning to try the Substack app, this is the time to do it.

Download the free Substack app (link below), log in with the email address you subscribe with, and my Notes appear in your feed, together with the full article archives and conversations.

The Substack app is a treasure and takes less than a minute to install on your phone.

Download Options:

• iOS Devices: Get it from the Apple App Store for iPhone and iPad.

• Android Devices: Download it from the Google Play Store.

If you’ve only ever read me in your inbox, there is a whole layer of this publication you haven’t seen yet.

So while I rest, there will still be short-form content from me most days. You’ll know where to find it.

I’ll see you back in your inbox in two weeks, with fresh energy and new exciting things coming your way.

Until then, take good care of yourself.

Anna

A reader sent this one in during a heavy training week. He finished with a line I hear constantly in the clinic: I assume I am undoing the whole thing.

The short answer

You are not. Eating more because you are hungrier does not cancel out the exercise. Hunger has a physiological basis, while two things work in your favour:

• On average, post-exercise eating replaces only part of the energy expended during training.

• Training improves your metabolic health through changes in the muscle itself. This has very little to do with the calorie arithmetic in the first place.

What’s happening in the body

In the hour or two right after an average training session, an aerobic class, a weight -lifting workout, or a run, interestingly, appetite goes down, not up. In a 2026 study in 58 overweight adults, a bout of high-intensity interval exercise reduced how much people went on to eat and lowered their appetite that day compared with a day when the same people rested instead [1].

Acylated ghrelin, a hormone that stimulates hunger, fell after vigorous exercise. At the same time, FGF21 and GDF15 rose: these hormones may help suppress appetite and reduce the drive to eat.

That suppression is brief. Hunger occurs a little later, to compensate for what was lost in terms of energy reserves: that evening, or the following morning.

You have already connected this hunger to your training days, and rightly so.

Between that early suppression and the hunger hours later, your muscle is restocking. Hard work during training uses much of the muscle’s glycogen, the form in which muscle stores carbohydrate.

For hours after you stop, the muscle keeps drawing glucose out of your bloodstream to refill that store, and it needs far less insulin than usual to do so, because the contractions themselves have moved the transporters that carry glucose into the cell up to the cell surface [2]. Refilling the store is prioritised and appetite increases across the following day while that refilling happens.

So the glucose streaming into your muscle is the benefit of the exercise, and the meal that follows a training session is key. The carbohydrate in that meal supplies the glucose the muscle is drawing in to rebuild its store, and because the transporters are already at the cell surface, glucose goes into the muscle reducing the amount stored as fat.

The protein is key during that time, as it supplies the amino acids the exercised muscle fibres use to repair themselves over the next day or two.

The relationship between feeling hungrier and actually eating more has been measured. In an analysis of 48 studies, people who exercised regularly for twelve weeks woke up hungrier - hunger measured before breakfast, on an empty stomach - yet their daily intake rose by only around 70 to 100 calories [3]. That is nowhere near enough to erase the work of the sessions [3]. A single session has the same effect: across the three days after one moderate intensity aerobic workout, people rated themselves hungrier while their actual food intake did not change [4]. The appetite rose but the eating behaviour barely followed.

Most people believe that the benefit of training is the deficit it creates: the calories burned. However, the truth is much more complex and interesting. A single session, moderate or hard, raises your insulin sensitivity for the next 24 to 48 hours. In plain terms, your muscle responds to insulin more readily, so it clears glucose from your blood faster and your body needs less insulin to keep blood sugar in range. Compared with where you were before the session, that sensitivity rises by up to 50% after moderate exercise, the pace at which you can still hold a conversation, and by more after hard exercise, the pace at which you cannot. And it rises whether or not you eat more afterwards [2].

Increased insulin sensitivity is the reason hunger cannot cancel out your training. This change cannot be affected by the increase in appetite.

The same plate of food is being handled by a changed body. Today the muscle draws in glucose readily and needs far less insulin to do it.

What I’d do (and do)

Eat in response to hunger on your training days, and add sufficient protein into the meal that follows each session. That meal reaches your muscle at the one moment it takes up glucose directly and is rebuilding the tissue that keeps you insulin sensitive.

The worth of a training session lies in what it changes inside you, far more than in the calories it spends.

Training remodels the muscle: it preserves and builds the tissue, and raises its capacity to take up and burn glucose. Muscle is metabolically active, so the more of it you carry, the more energy you use even at rest. Over months, your body composition follows the muscle, and the muscle can only rebuild when it is given the material to rebuild with, which is the job of that post-session meal.

One of my clients, a man in his fifties, was lifting three times a week, and cutting food back during training days because he interpreted hunger as greed. After seven months of doing that, his weight had not changed and his strength was declining. We changed what he ate after each session. Within about six weeks his strength recovered, and his body composition began to change for the first time that year.

If you have been eating as little as possible and finding that nothing improves, you may want to read why in [Four Things Change When You Eat Too Little After 40. Not One of Them Helps.]

If you want your own question answered, send it to me. It may well be the next note I write.

👉 If you enjoyed reading this, share it with friends!

References

1. Launbo NP, Jalking L, Jensen MM, Beaulieu K, Finlayson G, Blond MB, Wiggers A, Rungby J, Nilsson M, Wewer Albrechtsen NJ, Gerstenberg MK, Pedersen HE, Færch K, Grunnet LG, Salling J. Effects of exercise and exercise timing on energy intake and appetite control: a randomised crossover trial in people with overweight or obesity with and without type 2 diabetes. EBioMedicine. 2026 Jul;129:106353. doi: 10.1016/j.ebiom.2026.106353. Epub 2026 Jul 1. PMID: 42385612; PMCID: PMC13347617.

1. Bird SR, Hawley JA. Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport Exerc Med. 2017 Mar 1;2(1):e000143. doi: 10.1136/bmjsem-2016-000143. PMID: 28879026; PMCID: PMC5569266.

1. Beaulieu K, Blundell JE, van Baak MA, Battista F, Busetto L, Carraça EV, Dicker D, Encantado J, Ermolao A, Farpour-Lambert N, Pramono A, Woodward E, Bellicha A, Oppert JM. Effect of exercise training interventions on energy intake and appetite control in adults with overweight or obesity: A systematic review and meta-analysis. Obes Rev. 2021 Jul;22 Suppl 4(Suppl 4):e13251. doi: 10.1111/obr.13251. Epub 2021 May 5. PMID: 33949089; PMCID: PMC8365695.

1. Okada TE, Jeromson S, Rathwell S, Wright DC, Bomhof MR. Aerobic exercise elevates perceived appetite but does not modify energy intake over a 3-day postexercise period: A pilot study. Physiol Rep. 2024 Sep;12(18):e70066. doi: 10.14814/phy2.70066. Erratum in: Physiol Rep. 2026 Mar;14(6):e70821. doi: 10.14814/phy2.70821. PMID: 39328151; PMCID: PMC11427932.

Cover of TIME, 26 March 1984, showing two fried eggs and bacon arranged as a sad face beneath the headline “Cholesterol: And Now the Bad News…” The issue included an article on the silent progression of atherosclerosis and reported research that would later become personally significant in this story.

In 1953, American army pathologists began opening the chests of soldiers killed in action in Korea [1].

They were looking at their hearts. Those of three hundred young men. The men had been fit enough to be accepted for service and fit enough to be sent to a front line. None had a known history of coronary heart disease. Their average age was twenty-two.

The pathologists opened the coronary arteries along their length and looked inside.

In 77.3% of these young men, the artery walls were already thickened with atherosclerosis. In some, a vessel was narrowed by more than half [1]. I want to stress that these were not sick men. Nobody had flagged anything. Every one of them would have passed the medical tests of that era without comment. The developing disease that was already inside their arteries did not produce any symptoms, any complaints, and did not show up in any test.

That finding unsettled cardiology for a generation. It meant heart disease was not something that can happen only in the sixties. It had been under way since the twenties, invisibly, in men who were by every available measure well.

Sixty Years Later, the Same Examination

However, that is not the end of the story.

Between 2001 and 2011, military pathologists performed the same examination on 3,832 American service members who died in Iraq and Afghanistan [2]. Their mean age was 25.9. The method and population were broadly comparable.

This time the figure was 8.5%, while severe disease had fallen from 15% of them to 2.3% [1,2].

Seventy-seven down to eight and a half.

Nothing about human biology changed across those six decades. The exposures did.

Smoking is one important exposure the researchers identified. In 1980, 51% of American military personnel smoked. By 1998, 30% did [2]. The researchers name that fall in smoking as the most likely reason the arteries they examined were cleaner than the ones examined in 1953.

Average cholesterol levels also fell in the American adult population from the 1960s onward [3].

However, not everything improved.

Across those decades, the proportion of American adults with obesity rose from around 13% to more than 22% [4].

The criteria used today to classify arterial changes as disease are more precise than those applied in 1953, so fewer of those young soldiers may have now been described as having diseased arteries.

Even so, the central point remains: no one knew those changes were there. What mattered was what their arteries had been exposed to over the years. That is the difficulty. The process can continue for decades, influenced by what a person is exposed to, without producing a single symptom or abnormal test result.

I did not first come across this story in a textbook. Strangely enough, I heard about those young soldiers when I was about thirteen years old.

Where I First Heard About the Soldiers

At a kitchen table, from my father.

He was about forty-four. He had just had his second heart attack and came home with a list of instructions and very little explanation of how any of it had happened. So he began looking for answers. That is what I remember most clearly about that year: a man reading everything he could get hold of, trying to understand what had been happening inside his own body.

Somewhere in that reading he found the soldiers. I remember a copy of TIME magazine among the things he was reading. That issue contained an article about the slow, silent development of atherosclerosis. It may have been there that he first encountered the study [5]. He told me about those soldiers. I understood little about it then, but his amazement came through strongly. Boys of twenty-two, he kept saying. Already had heart disease.

He was asking for the thing his doctors had not given him. Not another test, and not another prescription. He wanted to know when it had started.

He never got that answer. He died of his third heart attack a few months before his fiftieth birthday.

The question he was asking is the one I have spent my working life on.

When does this disease actually start, and why is it not detectable before it is too late?

What Was Happening Inside Those Arteries

An artery’s inner lining is living tissue, one cell thick, and everything starts there.

That lining can be irritated by nutrition and lifestyle insults: tobacco smoke compounds that pass in the bloodstream, the mechanical force of high blood pressure against it, high blood glucose, and LDL particles that may penetrate the walls or become oxidised and reactant. And then an irritated lining may become more vulnerable and allow small LDL particles through into the arterial wall layers. Once inside, they are chemically altered, and the immune system treats the altered particles as debris and sends white cells in to clear them [6, 7].

The white cells take up fat, becoming foam cells, and accumulate in the arterial wall to form a fatty streak. As the lesion grows and inflammation continues, some cells die and leave behind cholesterol and cellular debris. In response, smooth-muscle cells migrate into the area and produce collagen and other fibrous tissue, forming a protective cap over the developing plaque.

This is common. When 2,876 people aged fifteen to thirty-four who had died of accidents, or other reasons were autopsied, every fifteen- to nineteen-year-old already had the earliest of these changes in the aorta, the body’s largest artery. More than half had them in the heart’s own arteries too.

However, they were discovered only because the arteries were examined closely in arteries after death. [8].

The pace at which those micro lesions advance into high-risk plaques varies enormously, and it is affected by cholesterol health, blood pressure, glucose and weight even at that age [8].

Why No Test Picked It Up

Here is what my father needed to know.

As plaque builds up in the wall, the artery does not narrow around it. It expands outwards. The whole vessel widens, and the channel the blood travels through stays the same width [9].

So blood flow stays normal. There is usually no chest pain, because pain arrives only when flow is restricted. An angiogram, which photographs the channel rather than the wall, can make an artery appear normal even when plaque is developing within its wall.

The vessel keeps making room until plaque occupies around 40% of the wall. Past that, there is no more room to give, and the channel finally starts to narrow [8].

So the tests that measure blood flow may appear normal throughout. These tests look for different consequences of disease rather than for early plaque within the arterial wall. A resting ECG may remain normal when the heart is not under strain. An exercise test looks for signs that blood supply becomes inadequate during exertion, while a conventional angiogram shows the width of the channel through which blood flows. As long as the artery expands outwards and preserves that channel, early plaque can therefore be present even when these tests show no evidence of narrowing.

The wall itself can be imaged. Ultrasound of the arteries in the neck or groin shows plaque directly, and a CT scan shows plaque that has hardened with calcium. Those tests look at the place the disease is, rather than the space beside it, and they can identify plaque before it causes symptoms or significant obstruction.

By the end of adolescence, many people already have early atherosclerotic changes in their arteries. What varies is their extent and the rate at which they progress.

Those soldiers were ordinary young men, examined in a level of detail that is possible only after death.

It Is Still Happening, and It Is Still Common

A Spanish study scanned the arteries of 4,184 people aged forty to fifty-four using two- and three-dimensional ultrasound to look for plaque in several arteries, together with CT scans to measure calcium in the coronary arteries. They were all free of symptoms and most at low calculated risk. The study found plaque already present in 63% of them [10].

For many apparently healthy middle-aged adults in Western populations, this is not unusual [10,11]. However, it is not ordinary everywhere.

Researchers scanned the hearts of 705 Tsimane adults in the Bolivian Amazon, aged forty to ninety-four, looking for the hardened plaque a CT scan picks up. Two thirds of those over seventy-five had none at all. Set against a large American population, their arteries were running about twenty-eight years behind [12].

They are probably not different physiologically than any of us. And they carry a heavy burden of infection and repeated inflammation, which should count against them. What they do have, however, is a lifetime of low LDL, low blood pressure, low blood glucose, no smoking and hours of walking every day [12].

So the speed at which plaque advances is not fixed by age, but it may be significantly affected by lifestyle. It depends on what the artery lining is exposed to, over years.

The Five Exposures That Change the Pace

The soldiers provide the answer. Two groups of young men were examined in the same way, sixty years apart. Their arteries had been exposed to very different conditions from childhood onward, and the contrast was striking: visible coronary plaque was found in three quarters of the earlier group, but in fewer than one in ten of the later group.

There’s strong evidence that five exposures may do most of the damage to the arterial lining:

Tobacco smoke, your own or other people’s. Its gases and particles increase oxidative stress and inflammation, reduce the availability of nitric oxide that keeps vessels functioning normally, and make the arterial lining more permeable and more prone to clotting. Smoking affects every stage of atherosclerosis, from the earliest endothelial injury to plaque rupture and thrombosis [13].

Blood pressure, the physical force pressing on the arterial walls. When that force remains high, it places repeated mechanical strain on the endothelium, reduces its ability to regulate vessel tone and promotes inflammation, LDL entry and remodelling within the wall. Blood pressure is not simply associated with cardiovascular disease: large randomised-trial analyses show that lowering it reduces the risk of major cardiovascular events across a wide range of starting levels [14]. If you are not measuring yours, it would be a good idea to start checking it.

LDL and other apoB-containing particles can enter and become retained in the arterial wall. Once retained, they may be modified and trigger inflammatory processes that contribute to plaque formation. The cumulative burden makes a difference: the more apoB-containing particles circulating, and the longer the exposure continues, the greater the opportunity for retention [6].

Blood glucose, which, when repeatedly or persistently elevated, increases oxidative stress, reduces nitric oxide, activates inflammatory pathways and makes the endothelial lining less able to control permeability and clotting. These changes help create conditions in which atherosclerosis can begin and progress, even before pre-diabetes or diabetes is diagnosed [7].

Chronic inflammation, meaning inflammation that stays switched on for years, rather than the kind that flares with an infection and then resolves. It may act on the lining independently of the other four exposures, so plaque can advance faster even when cholesterol and blood pressure are controlled.

Among 31,245 statin-treated participants in three trials, higher hsCRP - the blood test for inflammation - was a stronger predictor of cardiovascular death than higher LDL cholesterol [15]. When a medicine that blocks one inflammatory pathway was trialled, it lowered cardiovascular events without lowering LDL cholesterol at all [16].

In some people, testing the hsCRP marker can provide additional information about inflammatory cardiovascular risk, but it must be interpreted in the clinical context. Risk factors that may keep it raised include visceral fat, smoking, gum disease, broken sleep and untreated autoimmune conditions.

The Question You Can Still Ask

My father asked when it had started. Nobody could tell him, and nobody can give you a date either.

What you can do, is take your last three or four sets of results and place the same measurements side by side in date order: blood pressure, LDL and glucose. Do not look only at whether each result was inside the reference range. Look at the direction each one has been moving, how large the change has been, and how long that pattern has continued.

That is the best answer to his question that your health records can give.

He never got to ask it. You have time to.

Start by gathering every blood test you have had over the last ten years. A single result inside the reference range may tell you very little about when a process began. The same result shifting in the same direction across consecutive tests may tell you far more. Look for values that are gradually rising or falling, changes that persist from one test to the next, and several related markers moving together.

So, I could not stress this enough: request your historical records, place the same measurements side by side in one spreadsheet, and read across each row over time. This can show whether blood pressure, LDL, glucose or other markers have been moving towards greater risk long before any one result was labelled abnormal.

References

1. Enos WF, Holmes RH, Beyer J. Landmark article, July 18, 1953: Coronary disease among United States soldiers killed in action in Korea. Preliminary report. By William F. Enos, Robert H. Holmes and James Beyer. JAMA. 1986 Nov 28;256(20):2859-62. doi: 10.1001/jama.256.20.2859. PMID: 3534336.

2. Webber BJ, Seguin PG, Burnett DG, Clark LL, Otto JL. Prevalence of and risk factors for autopsy-determined atherosclerosis among US service members, 2001-2011. JAMA. 2012 Dec 26;308(24):2577-83. doi: 10.1001/jama.2012.70830. PMID: 23268516.

3. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL. Trends in serum lipids and lipoproteins of adults, 1960-2002. JAMA. 2005 Oct 12;294(14):1773-81. doi: 10.1001/jama.294.14.1773. PMID: 16219880.

4. Fryar CD, Carroll MD, Ogden CL. Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults Aged 20 and Over: United States, 1960-1962 Through 2013-2014. National Center for Health Statistics, Health E-Stats; 2016.

5. TIME. Medicine: Slow Death Without Fever. March 26, 1984;123(13). TIME Vault. Accessed August 5, 2026.

6. Borén J, Williams KJ. The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity. Curr Opin Lipidol. 2016 Oct;27(5):473-83. doi: 10.1097/MOL.0000000000000330. PMID: 27472409.

7. Yang DR, Wang MY, Zhang CL, Wang Y. Endothelial dysfunction in vascular complications of diabetes: a comprehensive review of mechanisms and implications. Front Endocrinol (Lausanne). 2024 Apr 5;15:1359255. doi: 10.3389/fendo.2024.1359255. PMID: 38645427; PMCID: PMC11026568.

8. Strong JP, Malcom GT, McMahan CA, Tracy RE, Newman WP 3rd, Herderick EE, Cornhill JF. Prevalence and extent of atherosclerosis in adolescents and young adults: implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth Study. JAMA. 1999 Feb 24;281(8):727-35. doi: 10.1001/jama.281.8.727. PMID: 10052443.

9. Onnis C, Virmani R, Madra A, Nardi V, Salgado R, Montisci R, Cau R, Boi A, Lerman A, De Cecco CN, Libby P, Saba L. Whys and Wherefores of Coronary Arterial Positive Remodeling. Arterioscler Thromb Vasc Biol. 2024 Dec;44(12):2416-2427. doi: 10.1161/ATVBAHA.124.321504. Epub 2024 Oct 31. PMID: 39479766; PMCID: PMC11594009.

10. Ibanez B, Fernández-Ortiz A, Fernández-Friera L, García-Lunar I, Andrés V, Fuster V. Progression of Early Subclinical Atherosclerosis (PESA) Study: JACC Focus Seminar 7/8. J Am Coll Cardiol. 2021 Jul 13;78(2):156-179. doi: 10.1016/j.jacc.2021.05.011. PMID: 34238438.

11. Nasir K, Ziffer JA, Cainzos-Achirica M, Ali SS, Feldman DI, Arias L, Saxena A, Feldman T, Cury R, Budoff MJ, Fialkow J. The Miami Heart Study (MiHeart) at Baptist Health South Florida, A prospective study of subclinical cardiovascular disease and emerging cardiovascular risk factors in asymptomatic young and middle-aged adults: The Miami Heart Study: Rationale and Design. Am J Prev Cardiol. 2021 May 28;7:100202. doi: 10.1016/j.ajpc.2021.100202. PMID: 34611641; PMCID: PMC8387278.

12. Kaplan H, Thompson RC, Trumble BC, Wann LS, Allam AH, Beheim B, Frohlich B, Sutherland ML, Sutherland JD, Stieglitz J, Rodriguez DE, Michalik DE, Rowan CJ, Lombardi GP, Bedi R, Garcia AR, Min JK, Narula J, Finch CE, Gurven M, Thomas GS. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. Lancet. 2017 Apr 29;389(10080):1730-1739. doi: 10.1016/S0140-6736(17)30752-3. Epub 2017 Mar 17. PMID: 28320601; PMCID: PMC6028773.

13. Ishida M, Sakai C, Kobayashi Y, Ishida T. Cigarette Smoking and Atherosclerotic Cardiovascular Disease. J Atheroscler Thromb. 2024 Mar 1;31(3):189-200. doi: 10.5551/jat.RV22015. Epub 2024 Jan 14. PMID: 38220184; PMCID: PMC10918046.

14. Blood Pressure Lowering Treatment Trialists' Collaboration. Pharmacological blood pressure lowering for primary and secondary prevention of cardiovascular disease across different levels of blood pressure: an individual participant-level data meta-analysis. Lancet. 2021 May 1;397(10285):1625-1636. doi: 10.1016/S0140-6736(21)00590-0. Erratum in: Lancet. 2021 May 22;397(10288):1884. doi: 10.1016/S0140-6736(21)01069-2. PMID: 33933205; PMCID: PMC8102467.

15. Ridker PM, Bhatt DL, Pradhan AD, Glynn RJ, MacFadyen JG, Nissen SE; PROMINENT, REDUCE-IT, and STRENGTH Investigators. Inflammation and cholesterol as predictors of cardiovascular events among patients receiving statin therapy: a collaborative analysis of three randomised trials. Lancet. 2023 Apr 15;401(10384):1293-1301. doi: 10.1016/S0140-6736(23)00215-5. Epub 2023 Mar 6. PMID: 36893777.

16. Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, Fonseca F, Nicolau J, Koenig W, Anker SD, Kastelein JJP, Cornel JH, Pais P, Pella D, Genest J, Cifkova R, Lorenzatti A, Forster T, Kobalava Z, Vida-Simiti L, Flather M, Shimokawa H, Ogawa H, Dellborg M, Rossi PRF, Troquay RPT, Libby P, Glynn RJ; CANTOS Trial Group. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017 Sep 21;377(12):1119-1131. doi: 10.1056/NEJMoa1707914. Epub 2017 Aug 27. PMID: 28845751.

This was a question that came in this week, from a reader who had looked it up, and found two opposing answers.

The short answer

On balance, helping, for both blood sugar and blood pressure.

Caffeine drives blood sugar and blood pressure in the wrong direction for an hour or two after you drink it.

However, long-term consumption of coffee as a whole drink, is associated with a lower risk of type 2 diabetes and of high blood pressure1.

Where it may work against you, the issue is usually the timing, the brewing method, and what else is in that cup.

What’s happening in your body

Caffeine works by blocking adenosine receptors. Adenosine is a compound that builds up in the brain across a waking day and produces the feeling of tiredness; the receptors are the docking points it acts on. Caffeine blocks those docking points, so the tiredness does not register and the nervous system stays stimulated. One consequence of that stimulation is a rise in adrenaline.

Adrenaline prompts the liver to release glucose and reduces how much glucose your muscle takes up, so for a couple of hours after a strong coffee your insulin sensitivity may be reduced2. The same nervous-system stimulation, together with caffeine’s effects on blood-vessel tone, can make the heart contract harder and temporarily raise blood pressure by several mm Hg for an hour or two.

That rise may get smaller the longer you have been a daily drinker. Regular users often develop partial tolerance, so the acute blood-pressure response may become smaller over time, although it does not disappear in everyone.

However, the bean is not only caffeine. Coffee also contains chlorogenic acids, which may influence intestinal glucose absorption and glucose metabolism by the liver. These compounds are among several possible explanations for coffee’s long-term association with lower diabetes risk.

Across more than a million people, compared with not drinking coffee at all, one cup a day was associated with around 8% lower risk of type 2 diabetes, three cups with around 21%, and five cups with around 29%. Furthermore, the heaviest coffee drinkers had around 7% lower risk of developing high blood pressure than the lightest drinkers (see footnote 1 the two studies).

So when someone sees their glucose monitor lift after a black coffee and concludes that coffee raises blood sugar, they are reading an adrenaline response which is brief, and does not reflect the long-term evidence.

If you have switched to decaffeinated coffee

Decaffeination does not remove the chlorogenic acids. In one trial the caffeinated cup carried 61 mg of them and the decaf cup 68 mg3 . The association was similar for caffeinated and decaffeinated coffee. The Ding study mentioned above analysed them separately and found no significant difference in their association with a lower risk of type 2 diabetes.

Switching to decaffeinated coffee substantially reduces caffeine exposure and may lessen the acute effects on insulin sensitivity, blood pressure, and protect your bedtime. If your blood pressure is not well controlled or caffeine leaves you feeling wired, decaffeinated coffee may be the better choice.

Decaffeination does not alter the effects of the brewing method, which is particularly important when considering coffee’s impact on cholesterol.

Cafestol and kahweol are two compounds carried in coffee oils, and they are still present in decaffeinated coffee. These compounds raise LDL cholesterol by suppressing bile acid production. A paper filter traps them.

Boiled coffee, Turkish or Greek coffee and cafetière coffee retain relatively high amounts of cafestol and kahweol. Espresso also contains them, although the amount consumed per serving is generally smaller. Paper-filtered coffee contains much less.

In intervention trials, substantial consumption of unfiltered coffee has raised LDL cholesterol, sometimes by several tenths of a mmol/L compared with filtered coffee or control drinks4.

So, if cholesterol is your concern, add a filter.

What I’d do

Drink coffee after breakfast, not before. In a small study, strong black coffee after a disrupted night increased the blood sugar response by about 50%, compared with the same broken night and no coffee5.

Complete drinking your coffee by early afternoon. Caffeine’s average half-life is about five hours, although it varies considerably. With a five-hour half-life, roughly one-third of a 4 p.m. dose would still be present at midnight, disturbing the sleep that affects your insulin sensitivity until the following day6.

Be mindful of what goes in your cup. Three large US studies compared people by what they added to their cup7 . Black coffee showed the strongest association with a lower risk of type 2 diabetes. Adding a teaspoon of sugar per cup appeared to weaken that association by about half, while artificial sweeteners weakened it by about a third. Cream did not appear to make any difference.

If blood pressure is your concern, do this: take a reading before your coffee and again 60 to 90 minutes after, on a few separate days. People clear caffeine at very different rates, so your own readings will help you see what your own body’s response is.

Blood pressure starts rising about 30 minutes after coffee, may peak between 60 and 90 minutes, and is usually back to baseline within two to four hours. Measuring at 30 minutes would catch it on the way up rather than at its height.

One client came to me drinking two black coffees before eating anything, with morning glucose readings that stayed high until lunch. We changed the timing: she began having breakfast and coffee together instead of drinking coffee on an empty stomach. Her morning readings came down within two weeks.

Adrenaline is not the only stress hormone that raises blood sugar this way. Cortisol can also increase glucose availability, which is what I cover in the article You Wake Too Early. Relaxing Will Not Fix It, about cortisol and blood sugar.

In summary, most people do not need to give up coffee. If caffeine raises your glucose or blood pressure, consider having coffee with or after breakfast, reducing the dose or choosing decaf. Avoid caffeine late enough in the day to protect your sleep, limit added sugar, and choose paper-filtered coffee if LDL cholesterol is a concern.

If you want your own question answered, send it to me. It may well be the next note I write.

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A husband and wife in their fifties came to see me. Both had noticed their waistline increase over the past few years. They had not changed their diet. It had always been home-cooked meals.

She had been told it was the menopause. He had been told it was his age.

Two different explanations, for a similar change. Neither offered any guidance on what could be done about it.

When your waistline changes, you almost certainly ask: What have I started doing that caused this?

It made no sense

To understand what may be behind this change, it helps to look at a rare case that stripped the question down to bone.

A 29-year-old man arrived at a clinic carrying weight around his middle that did not match a body that age1. His waist was thick. A scan showed his liver was marbled with fat. His blood sugar had already developed into type 2 diabetes. The skin under both arms had darkened into velvety patches, a change that appears when insulin has been running high in the blood for a long time.

None of it fit. He was not a heavy eater. And when a man carries fat around the middle like this, the hormone we tend to think about first is testosterone, because a shortage of it is a known cause of exactly this pattern in men. So they measured his. It was normal, if anything, high.

They tried testosterone treatment regardless. His metabolic markers got worse. The insulin resistance increased, the diabetes remained the same.

Then they tried a hormone nobody expects to give a young man. They gave him oestrogen.

His insulin resistance improved. The fat in his liver receded. His blood sugar dropped. Two plaques that had formed in his carotid arteries disappeared.

Genetic testing showed that his body could not produce oestrogen. A mutation in a single gene had knocked out aromatase, the enzyme that turns testosterone into oestradiol. So despite all that testosterone, he had almost no oestrogen in circulation.

The fat around his middle, the fat in his liver, and his high insulin had all been kept in check, in a man, by oestrogen, the hormone most people think of as a female hormone.

His condition is extremely rare. But it shed light on something that applies to everyone, including the couple in my consulting room.

Fat deposition and insulin sensitivity are not just results of how a person lives, though we tend to reduce them to that. They are actively controlled by hormones, and where that control is absent, for whatever reason, the waist is prone to expand.

A change the scale cannot reflect

Now back to the wife, and to one useful piece of research in this field.

Greendale and colleagues2 , followed 1,246 women through the menopause transition, scanning them repeatedly with DXA, a body scan that measures fat, muscle and bone. The scans showed something interesting. The rate of fat gain doubled, from 0.25 kg a year before the menopause transition to 0.45 kg a year during it.

So, at the same time, the woman’s muscle mass reversed direction, from a slight yearly gain into a yearly loss. Fat was being added and muscle taken away at the same time.

All of this happened inside a specific window: roughly two years before her final period through to about eighteen months after it.

Her body composition shifted over about three and a half years.

Her brake: oestradiol

Oestradiol restrains fat accumulation and influences where fat is deposited. During the transition her oestradiol drops sharply. Her androgens, the male-type hormones women also make in smaller amounts, fall far less, so the balance between the two tips toward the androgens. A lower oestrogen-to-androgen balance is associated with more visceral fat, the deep fat around the organs, and less of the subcutaneous fat that used to be stored in hips and thighs3.

Her fat did not just increase. It relocated to the abdomen. And the abdomen is a key site that drives insulin resistance.

His brake: testosterone

Testosterone provides similar protection in a man, and he loses it too. Men do not have a menopause, but their testosterone declines gradually, from around the age of 40, and faster if weight is gained4 . The decline is easy to miss, which is part of why the waist is often the first thing he notices.

Testosterone prevents fat storage through two routes at once.

The first route is direct. Fat cells begin as unspecialised cells that later mature into fat-storing ones. Testosterone, and its stronger relative dihydrotestosterone (DHT), interrupt that process: they stop those young cells from becoming mature fat-storing cells in the first place5 . These hormones act through receptors on fat cells. Those receptors are more common in deep abdominal fat than in the fat just under the skin, so testosterone may have its strongest effect where visceral fat tends to build.

The second route runs through oestradiol. A man makes his oestradiol from his own testosterone, and he needs it: in men, oestradiol helps hold body fat down and supports bone strength and libido.

In a study of 400 men6 whose own hormone production was suppressed and then replaced at graded doses, how much body fat a man gained depended on his oestradiol level; while his muscle mass, thigh size and leg strength depended on his testosterone. When the body was prevented from turning testosterone into oestradiol, the men gained more body fat at every testosterone dose. This showed that oestradiol helps limit fat gain in men, independently of testosterone.

The young man in the published clinical case, had lost only one of these two routes: the oestrogen one. A midlife man losing testosterone loses both at once: the direct brake testosterone puts on fat cells, and the oestradiol his body would have made from it.

Low testosterone and visceral fat can reinforce each other. The testes may produce less testosterone with age, while excess weight may disrupt the brain signals that tell the testes to make testosterone. In a study of 3,369 men7, carrying excess weight was linked to about three times the risk of developing this second form.

Fat tissue contains aromatase, an enzyme that converts testosterone into oestradiol. As abdominal fat increases, this conversion may increase and, in some men, stronger oestradiol signalling may further suppress testosterone production. This can create a cycle: more abdominal fat may lower testosterone, while lower testosterone may make further fat gain easier by reducing muscle mass and weakening the restraint on fat storage.

Oestradiol’s role in men can therefore seem contradictory. At normal levels, it helps limit fat gain. But when excess abdominal fat alters the balance between oestradiol and testosterone, the overall effect may work against him.

The practical solution is clear. In a review of 24 studies, a low-calorie diet raised total testosterone, and weight-loss surgery raised it about three times as much8 .

In both the man and the woman, declining sex-hormone activity may have weakened those main controls of abdominal fat accumulation. Hers was oestradiol affected by menopause. His was testosterone.

His hormone problem may be corrected by reducing abdominal fat. Hers cannot. But she can still act on what the lower oestradiol is doing to her muscle and her insulin sensitivity.

Other forces affect these changes too: thyroid disease, and some common medications, such as corticosteroids like prednisolone and certain antidepressants, which alter body fat and metabolism on their own.

Sleep loses hormonal support too

In the cortisol article, I described early-hours waking as a potential nocturnal glucose dip pulling up cortisol and adrenaline, and said the hormonal half of that story had its own article ahead. This is it.

For her, the broken night is a combination of two factors.

Falling asleep is very much a progesterone story in women. The body converts progesterone into a calming compound that acts on the brain’s main quietening system (the GABA-A receptor), the same system sedative medicines work on. As progesterone declines during menopause, that sedative support is gone9 .

Waking too early in the morning is an oestradiol story for women. Oestradiol helps regulate body temperature, partly by widening the small blood vessels near the skin so the body can release heat. As it falls, night sweats and hot flushes produce repeated arousals; and rising follicle-stimulating hormone (FSH) with falling oestradiol is associated with more time awake after sleep onset and more fragmented sleep. The cortisol pattern then adds one more layer to the problem.

For him, the loop runs in the opposite direction where sleep quality affects testosterone levels. Factors including obesity, sleep apnoea and stress may affect sleep. Leproult and Van Cauter10 restricted ten healthy young men to five hours in bed for eight nights. Their daytime testosterone fell by 10 to 15 per cent. Testosterone may decline naturally at roughly 1 to 2 per cent a year, so the effects of one week of short sleep can be compared to those of a decade of ageing.

His broken night works both ways. It can increase appetite and worsen insulin sensitivity, making fat gain more likely. That extra fat may then contribute to lower testosterone, while lower testosterone can further weaken the body’s restraint on fat storage.

Finding your cluster

These clusters can help you identify patterns, but they cannot diagnose a condition. The symptoms overlap, and persistent or significant changes may require clinical assessment and appropriate testing.

The sex-hormone cluster:

For a woman: if the abdominal weight developed together with hot flushes, night sweats and cycle changes, and appeared over a defined few years, the sex-hormone cluster may be driving it.

For a man: if abdominal weight gain developed together with a reduction in libido, over a defined period, the sex-hormone cluster is the place to look.

The cortisol cluster:

If instead the weight followed early-hours waking, stressful days, or prolonged life life pressure, look at the cortisol cluster first.

The blood-sugar cluster:

If the abdominal weight occurred with post-meal energy dips, rising fasting glucose or triglycerides, and cravings that build through the afternoon, the blood sugar imbalance is the place to start.

Note that most people have more than one cluster running. The question you need to answer is which ones may be predominant right now.

Get ready to act on what has changed, with clear steps below for both women and men. You also get access to the clustering guide, which helps you work out which pattern is yours and what to do about it, using your own results.

Read more

This question came in from a reader last week, and it is one of the questions I hear most in clinic. Fruit has somehow been reclassified as something to fear.

The short answer

No. You do not have to give up fruit, and for most people with insulin resistance, cutting it out completely is the wrong move. Whole fruit, in sensible amounts, belongs in your diet.

What changes how your body responds is the form the fruit comes in and how you eat it, far more than the sugar it contains.

What’s happening in your body

When you eat a whole apple, the glucose and fructose inside it are held within the fruit’s cell walls and its soluble fibre. That fibre reduces how fast your stomach empties and how quickly those sugars reach your bloodstream, so the rise in blood glucose is gentler and more gradual than someone would expect based on the sugar content.

Juice removes that protective structure. The fibre is stripped out, the sugars are freed, and they are absorbed in the bloodstream quickly, which is where the sharp glucose rise and the insulin response behind it come from. Dried fruit, on the other hand, concentrates the same sugars into a small volume, so it is easy to overeat.

Fruit also carries a share of fructose, which your liver processes. In small doses from whole fruit, fructose is handled easily. In large loads, from juice, dried fruit, or several servings of very sweet fruit at once, such as overripe fruit, the liver converts more of it into fat, and that may contribute to insulin resistance.

So, the form, the amount and the ripeness are the three factors you need to take into account.

Berries and the skins of many fruits are rich in polyphenols: natural plant compounds that may help the body manage glucose more effectively. Polyphenols may slow the digestion and absorption of carbohydrates and support the cells take up glucose from the bloodstream more efficiently.

So the blanket claims that fruit is sugar and sugar is sugar, treats an apple as though it were a glass of juice or a spoonful of table sugar. It ignores the fibre, the dose, and the form, the three things that determine the response.

What I’d do

Keep whole fruit in your diet, and choose it well. Select higher-fibre, lower-sugar options such as berries, apples, pears, citrus, and kiwi, and avoid large portions of very sweet or overripe tropical fruit. Eat fruit whole rather than juiced. Pair it with protein or fat, or have it as part of a meal rather than alone on an empty stomach. This way, the glucose rise is blunted further. Be cautious with dried fruit and smoothies, where several servings slip in without your noticing.

One client arrived having cut fruit out entirely for a year. Her glucose had not improved, her fibre intake had dropped, and her sweet cravings had increased. We reintroduced a handful of berries with Greek yoghurt, which satisfied her cravings and increased her fibre intake. With the gradual reintroduction of the right amounts of fruit, she saw a significant improvement in her blood sugar.

Fruit is only one part of the picture. You may also want to find out why reducing your overall insulin load matters more than focusing on a single glucose reading. To learn more, read this article: [You Lowered Your Blood Sugar. So Why Hasn’t Anything Changed?].

So, keep the fruit. Change the form, mind the amount, and let the fibre do its work.

If you want your own question answered, send it to me. It may well be the next note I write.

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Life magazine photograph of conscientious objector being examined on a tilting table during starvation experiment. July 30,1945. Volume 19, Number 5, p. 45. Credit: Wallace Kirkland/Time Life Pictures/Getty Images (Kalm and Semba, 2005).

In November 1944, in a laboratory built into the vaults beneath the football stadium at the University of Minnesota, thirty-six young men were fed meals containing about half the food their bodies needed.

They had volunteered for it. During the war a recruitment brochure had circulated among conscientious objectors. Its cover showed three hollow-cheeked children staring down into empty bowls, and above there was this question: Will you starve (so) that they be better fed? More than four hundred men said yes. Thirty-six were chosen, the fittest and healthiest of the applicants, they were examined and declared medically fit.

For the next six months the men lived on turnips, swede (rutabaga in the United States), macaroni, and dark bread. And their bodies began to change in ways the researchers had not entirely foreseen.

They grew gaunt. They felt cold in a heated room. They turned listless and irritable and could not hold a thought for long. Above all they became consumed by thoughts of food, reading cookbooks for hours, hoarding recipes they had no means to cook, drawing out every mouthful of food they were given. Their heartbeats became slower. Their resting metabolism fell by around 40%1. This means that their bodies started using about 40 per cent less energy while at rest.

That was the physiological response of their bodies to the energy deficit.

Nobody today is living on swede in a basement laboratory. But a similar version of the same mechanism runs in anyone who has eaten too little for too long. The body adapts to preserve energy.

Those men showed that these adaptations can result from the calorie deficit, not from any particular age or health state. However, as we age, the consequences of these adaptations are heavier and harder to reverse. There is less muscle in midlife, and rebuilding it requires more effort. The resting metabolic rate (=the energy your body uses while at rest) is already lower than it used to be. Oestrogen in women and testosterone in men are falling during this phase of life, and these hormone changes accelerate the loss of muscle. So, the challenge of under-eating can lead to greater muscle loss than it would at a younger age, as well as a lower resting metabolic rate.

You might be counting on the same arithmetic yourself. Eat less, weigh less.

You have reduced the bread. Minimised the portions. Maybe you skipped breakfast. The plates became smaller and the hunger louder, and still the weight would not come off. The scales settled at a number and stayed there. The same waistband, still tight.

Months, even years of eating less, and the weight will not move. So you ask:

I am barely eating anything. What is there left to cut?

The Assumption Underneath the Advice

It is a reasonable question. Very logical: If you are overweight, eat less. If eating less has not worked, you are still eating too much, so reduce it further. Cutting further feels like the only lever left.

But for anyone in midlife, woman or man, who has been under-eating for years, eating less is frequently the reason the numbers hold where they are.

A long energy deficit sets four adjustments running. Each one is the body responding sensibly to less fuel. Together they work against the exact result you have been chasing, and beyond a certain point, individual metabolic and hormonal adaptations drive much of the difference between who loses and who does not2.

The First Thing to Go Is Heat

When energy coming in stays low for long enough, the amount you burn at rest comes down. Researchers call it adaptive thermogenesis, and it is measurable within the first week of eating substantially less. In one controlled study, resting energy expenditure dropped by roughly 100 calories a day after only seven days of heavy restriction, and those whose metabolism dropped the most lost the least weight in the end3.

This lower expenditure is normal physiology. When the body is given less fuel, it spends less. The reduced rate can also outlast the diet. The longer the deficit has run, the longer the reduced rate tends to be maintained. In some people it stays low even after normal eating returns4.

And then there is the second factor.

The Second Is the Hormone That Sets the Pace

The thyroid sets the pace of your metabolism, meaning how fast your cells turn fuel into energy, how much heat your body produces, and how hard your heart works at rest. It does this largely through T3, the active form of thyroid hormone. Most T3 is not produced by the thyroid directly. It is converted from the storage form, T4, out in the tissues. Prolonged energy restriction reduces that conversion.

In one study, twelve months of modest weight loss lowered circulating T3 significantly while the standard thyroid tests, TSH and free T4, barely changed5. This is what most blood panels miss. A doctor reading a normal TSH may reasonably conclude the thyroid is fine, while the active hormone that sets the metabolic pace has come down. Lower T3 means a lower resting rate, more sensitivity to cold, flatter energy, and a system running at reduced output.

The Third Is a Stress Response

Running on very little food is itself a physiological stressor, and the body responds to stressors through cortisol.

Significant restriction and prolonged fasting raise cortisol. A meta-analysis of thirteen studies found the effect strong for fasting, and weaker or absent for gentler calorie reduction6. But cortisol can climb even with everyday dieting. In one controlled study, people who counted and cut their daily calories showed higher cortisol and reported feeling more stressed7.

Higher cortisol pushes glucose up through the liver and works against insulin. So, paradoxically, the more you cut back, chasing a weight that will not shift, the higher your fasting blood sugar may rise.

The Fourth Is the Tissue You Most Need to Keep

When protein and total energy both stay low, the body draws on muscle for fuel. Muscle is expensive to keep and easy to release, and in a deficit without enough protein, or enough demand to keep it, it goes.

That loss carries a metabolic cost far beyond strength. Skeletal muscle is the largest site of glucose disposal in the body8. It clears sugar from the blood, including through routes that do not depend on insulin. By losing muscle you lose the tissue that keeps your cells insulin-sensitive.

The encouraging part is how modifiable this one is. In a controlled trial, people in an energy deficit who ate substantially more protein and trained against resistance gained lean mass and lost fat at the same time9. The calorie deficit did not have to cost them muscle. What they ate, and how they moved, determined whether it did.

Four Changes, All Pointing the Same Way

Take the four effects of calorie restriction together: lower resting rate, lower T3, higher cortisol, less muscle. Each one predisposes the body towards preserving energy rather than releasing it, and towards higher blood sugar rather than lower.

These were the same changes that overtook the men in Minnesota: the collapse in resting metabolism, the cold that persisted - signs of thyroid hormone metabolism changes, the muscle wasting from their frames. In them, it was severe and clear to see. In a mild, sustained deficit the same adaptations happen but are subtle and may remain hidden, which is what makes them so easy to miss.

You might reasonably ask why those men lost weight, when the argument here is that eating too little holds the weight in place. They did lose weight, plenty of it. But to keep it coming off, they had to keep cutting back. As their metabolism fell, the same rations stopped producing the same loss, and the researchers had to keep reducing their food10.

That falling metabolism is the adaptation. Six months in, the Minnesota men were still in its early phase, still losing. Someone who has spent years under-eating has been in that state long enough for the body’s adaptation to settle in. Intake and output are even, and the weight stops changing.

So your food diary looks as though it should guarantee weight loss, while the scale remains stubborn and the blood markers may not improve.

The effort is heroic. The food intake really is minimal. The return on that effort has been turned against itself by a system defending its reserves.

In midlife there is often a further hormonal layer, and it runs differently for women and men. If you are a woman, falling oestrogen accelerates muscle loss and changes where fat is stored11. If you are a man, declining testosterone does much the same, by a different route.

Either way it compounds every one of the four changes above. In this respect, women and men are more alike than they are different. Genetics, years of metabolic strain, hormonal changes, medication, thyroid imbalances: all of these affect the numbers together with anything you eat or do.

What Eating Enough Actually Does

Eating enough, and eating enough protein in particular, reduces the pressure to break down muscle for fuel, supports the conversion of T4 into active T3, and lowers the stress load that keeps cortisol raised. This is central in protecting the metabolic rate.

Protein at each meal gives the body less reason to take from muscle. Enough total energy intake reduces the need to conserve. Resistance work then gives muscle a reason to stay. Together, these three move the four adverse effects of under-eating in the opposite direction.

You do not have to have been diagnosed with anything, for the same four changes to be happening to you. They take hold of anyone who eats too little. So if your blood test results still read normal, and you assume that eating less is always the safer choice, you are counting on the same flawed arithmetic.

So here is the permission: you are allowed to stop eating less.

It is natural to fear that eating more can only mean gaining weight. But if a long deficit is what has kept the weight from moving, recovery has to start differently: with enough food, enough protein, and resistance work introduced together. These are the conditions that allow your resting metabolic rate to rise again, protect the muscle that helps clear glucose, and bring cortisol and insulin down.

Go gradually. If you have been eating very little for a long time, a sudden jump to large meals can land as fat gain, because your metabolic rate is reduced to meet your low intake. Add food back in small steps over a few weeks, and start resistance work at the same time, so the extra energy goes into rebuilding muscle rather than into storage.

Expect the scale to rise a little at first, since much of that early weight is water and refilled muscle glycogen, not fat. Judge the change over months, by how your clothes fit, your strength, and your energy, rather than by the number each morning.

Together these are the conditions in which the body can release fat instead of holding on to it.

The hunger you have been overriding was accurate all this time. You were actually short of fuel. Eating enough is the work itself, the thing that will allow the weight to move.

The Reverse

The guidance here is the reverse of the one you have been following for years, and, I know, it asks something even more challenging than restraint. It asks you to trust that feeding yourself is the intervention. I get how this is tough to accept.

If eating less and less has taken you nowhere, the smartest question is not how much more to take away.

The focus should be on what has been missing that made weight loss almost impossible.

The appointment lasted about ten minutes.

Your results were reviewed. A number was too high, or perhaps two were. The doctor explained what the medication would do. The prescription was written and handed across the desk.

You left with the sense this had been resolved.

And in one sense it had. The number will come down. The scientific evidence behind that drug is real. The prescription was the right call, and the risk it manages is real.

But the process that raised the number in the first place did not stop when you received the prescription.

The Medication Does What It Says on the Label

Statins, antihypertensives and other drugs are meant to manage measurable cardiovascular risk factors. These drugs are well-studied, effective, and for many people may be necessary and life-saving. If your doctor prescribed one, there was a good reason and the aim was to reduce the risk of complications.

However, the assumption that because a number is now being managed, the underlying imbalance or dysfunction has been addressed is a false sense of resolution.

It has not been addressed.

A prescription targets a marker. It may not target the mechanism that produced it.

The gap between a marker and a mechanism is easiest to see in two drugs almost everyone in this position has been handed: the statin for cholesterol, and the tablet for blood pressure.

Take the statin first.

What a Statin Actually Does Inside the Body

Statins, meant for cholesterol management, work by blocking a specific enzyme in the liver’s cholesterol production process. When that enzyme is blocked, the liver compensates by increasing the number of receptors on its surface that capture and remove LDL particles from circulation. The result is a measurable reduction in serum LDL.

In people with cardiovascular disease, the evidence for benefit is robust. Beyond cholesterol-lowering, statins also appear to have modest anti-inflammatory effects. The JUPITER trial, published in the New England Journal of Medicine in 2008, found that statin therapy reduced levels of hsCRP, a marker of systemic inflammation, in people with elevated levels. Statins may also help to make existing plaques in artery walls more stable, reducing the likelihood of rupture.

These are significant effects.

However, a statin is not meant to address the insulin resistance that, in many people with high cardiovascular risk, is driving cholesterol imbalances in the first place.

In the presence of insulin resistance, the liver produces more triglycerides, which changes how LDL cholesterol particles are packaged. Instead of larger, relatively buoyant LDL particles, the liver produces smaller, denser ones. These smaller, denser particles are more likely to penetrate artery walls and trigger the inflammatory process and plaque formation.

A statin will usually lower LDL cholesterol and often reduce apoB-containing particles in circulation. It may not correct the fact that insulin resistance is producing a more damaging particle profile.

There is also evidence that statin use may increase blood sugar in some people, particularly those already near the diagnostic threshold for diabetes. A 2024 meta-analysis by the Cholesterol Treatment Trialists’ Collaboration, that combined data from nineteen placebo-controlled randomised trials and four trials comparing statin intensities, involving 154,664 participants, reported that statin therapy may cause a moderate, dose-dependent increase in new diagnoses of diabetes. The effect was more pronounced with intensive-dose therapy. For someone already navigating insulin resistance, this is worth knowing, and it is a reason to broaden the strategy to include nutritional and lifestyle interventions that support metabolic health.

What an Antihypertensive Actually Does Inside the Body

Blood pressure medications work on the pressure problem rather than the root causes that cause it. The different classes, whether they work by relaxing blood vessel walls, reducing the volume of fluid in circulation, or slowing the heart rate, share a common logic: they intervene in the final pathways that produce elevated pressure readings.

That intervention works.

Blood pressure comes down.

The risk of complications associated with sustained high blood pressure, particularly stroke, heart failure, vascular damage, and progressive kidney disease, falls.

But elevated blood pressure in the context of metabolic imbalance is not primarily a problem of too much pressure.

The blood vessels have become less able to handle pressure well.

Every blood vessel has a very thin inner lining that we call the endothelium that helps control how relaxed or tight the vessel is. One of the key ways it does this is by making nitric oxide, a natural compound that tells blood vessels to relax and stay flexible.

When the endothelium is exposed to the metabolic stress that often comes with insulin resistance, such as inflammation, high blood sugar, and oxidative stress, it produces less nitric oxide. As a result, blood vessels become less flexible, blood flows less easily, and blood pressure may rise.

An antihypertensive will reduce the pressure reading. But it does not, by itself, repair the blood vessel lining, address the inflammation and oxidative stress that damaged it, or undo the blood vessel stiffening that can build up when the underlying metabolic problems are left unaddressed.

It is also worth knowing that not all blood pressure medications are equal. Older beta-blockers and certain diuretics may modestly worsen blood sugar regulation and insulin resistance.

ACE inhibitors and ARBs, two other common classes, appear more metabolically neutral, and some evidence suggests a modest benefit for insulin sensitivity.

The Shared Gap

Two different medications. Two different numbers, both brought under control.

And underneath both, the same imbalance is still running.

Insulin resistance, chronic low-grade inflammation, oxidative stress, excess visceral adipose tissue. This imbalance responds to what you eat and how you live.

Statins and antihypertensives were never designed to address it.

It is not neutralised by your prescription.

But this is the fact often missed. The very drivers the drugs cannot reach are the ones you can. Nutrition and lifestyle act on that underlying process directly, while the medication holds the number and lowers your risk.

The Levers Still in Your Hands

This is the work medication does not do for you. But this work is within your reach.

Endothelial function responds to diet.

Foods that support the production of nitric oxide, particularly leafy green vegetables, beetroot, and polyphenol-rich foods such as berries and extra-virgin olive oil, give the endothelium what it needs to do its job.

Omega-3 fats, found primarily in oily fish such as salmon, mackerel, sardines, and anchovies, directly support endothelial function.

Studies suggest that omega-3 supplementation may help blood vessels relax more easily. Researchers often measure this using a test called flow-mediated dilation, which looks at how well an artery widens in response to increased blood flow.

In a study of statin-treated coronary artery disease individuals, EPA, an omega-3 fatty acid derived from fish oil, improved endothelial function most clearly in those with high triglycerides.

The republished PREDIMED trial, in 2018, found that a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced major cardiovascular events in people at high cardiovascular risk compared with a reduced-fat diet.

A 2024 umbrella review of 18 meta-analyses, covering 238 clinical trials, found that Mediterranean-style dietary interventions were associated with lower fatal and non-fatal cardiovascular outcomes.

A 2026 review comparing Mediterranean and low-fat dietary patterns reported more favourable effects for the Mediterranean diet across several cardiometabolic markers, including lipids, inflammatory markers, blood pressure, and insulin sensitivity.

A large proportion of the populations studied were already on medication. The dietary benefits were additional to it.

Lipid quality, not just lipid quantity, responds to diet

The small dense LDL pattern is not usually corrected by statins alone and is strongly influenced by triglycerides, insulin resistance, carbohydrate quality, fibre intake, weight change, and the balance of saturated and unsaturated fats in the diet.

When refined carbohydrates are replaced with fibre-rich whole foods, and saturated fats are swapped for healthier unsaturated fats from foods like olive oil, nuts, seeds, and oily fish, the overall blood-fat profile can improve in ways beyond the quality of LDL cholesterol.

Soluble fibre, found in oats, legumes, and vegetables and fruit, also binds cholesterol in the gut, reducing the amount recirculated into the bloodstream.

Are your cells sensitive to insulin?

Insulin sensitivity means how well the body responds to insulin, the hormone that helps move sugar out of the blood and into cells for energy. When insulin sensitivity improves, the body does not have to work as hard to keep blood sugar controlled.

Diet and movement can improve this. Even modest changes, such as eating fewer refined carbohydrates, eating enough protein and fibre, and building regular physical activity into daily life, can improve several markers at once. Triglycerides can fall, HDL function can improve, inflammation may decrease, and blood pressure can become easier to manage.

Blood pressure responds to dietary minerals

The original DASH trial, published in the New England Journal of Medicine in 1997, established that a dietary pattern rich in potassium, magnesium, and calcium and low in sodium produces clinically significant blood pressure reductions.

Systematic reviews and meta-analyses have found that the DASH diet significantly reduces systolic and diastolic blood pressure and can improve lipid markers, including total and LDL cholesterol.

Lowering blood pressure is not only about eating less salt. It is also about improving the balance between sodium and potassium. Most Western diets are high in sodium and low in potassium, which can make blood pressure harder to control.

Potassium-rich foods such as vegetables, legumes, nuts, and seeds can help restore that balance naturally. This supports blood pressure control and can work alongside medication rather than against it.

The Markers Sitting Just Outside the Flag

If you are on a statin, directly relevant markers worth watching alongside LDL include:

• Triglycerides and HDL cholesterol. Together, these give a picture of insulin resistance and lipid particle quality. A high triglyceride-to-HDL ratio is a useful indicator that small dense LDL particles are likely predominant.

• Fasting glucose and, ideally, fasting insulin. These help track how well the body uses and manages glucose, which affects cholesterol metabolism in ways a statin does not directly address, and are worth monitoring given the dose-dependent relationship between statin use and blood sugar changes.

• High-sensitivity CRP. An indicator of systemic inflammation. A statin may lower it, but diet can lower it further, and knowing your baseline is useful.

If you are on an antihypertensive, directly relevant markers worth watching include:

• Fasting glucose and insulin, for the same reason as above.

• Kidney function markers, because some blood pressure medications affect kidney filtration and electrolyte balance, and this is routinely monitored but worth understanding.

• Electrolytes, particularly potassium. Some antihypertensives deplete potassium, which affects both blood pressure regulation and broader metabolic function.

These markers can be discussed with your doctor as additional context for understanding the whole picture.

The Prescription Is Not the End of the Conversation

The medication handles one variable. The mechanism that produced it is still affected by everything you eat, how you move, how you sleep, and how much load your body is carrying.

None of that is outside your reach.

The prescription and the nutritional and lifestyle work can complement each other. One keeps the number within range and lowers your risk today. The other works on the mechanism underneath, over months.

They aim at different targets, on different timescales.

References

Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med. 1997 Apr 17;336(16):1117-24. doi: 10.1056/NEJM199704173361601. PMID: 9099655.

Arabi SM, Bahari H, Chambari M, Bahrami LS, Mohaildeen Gubari MI, Watts GF, Sahebkar A. Omega-3 fatty acids and endothelial function: A GRADE-assessed systematic review and meta-analysis. Eur J Clin Invest. 2024 Feb;54(2):e14109. doi: 10.1111/eci.14109. Epub 2023 Oct 19. PMID: 37859571.

Bekbossynova M, Saliev T, Ivanova-Razumova T, Andossova S, Kali A, Myrzakhmetova G. Small dense LDL: An underestimated driver of atherosclerosis (Review). Mol Med Rep. 2025 Dec;32(6):328. doi: 10.3892/mmr.2025.13693. Epub 2025 Sep 26. PMID: 40999979; PMCID: PMC12512508.

Cholesterol Treatment Trialists’ (CTT) Collaboration. Electronic address: ctt@ndph.ox.ac.uk; Cholesterol Treatment Trialists’ (CTT) Collaboration. Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis. Lancet Diabetes Endocrinol. 2024 May;12(5):306-319. doi: 10.1016/S2213-8587(24)00040-8. Epub 2024 Mar 27. PMID: 38554713; PMCID: PMC7615958.

Estruch R, Ros E, Salas-Salvadó J, Covas MI, Corella D, Arós F, Gómez-Gracia E, Ruiz-Gutiérrez V, Fiol M, Lapetra J, Lamuela-Raventos RM, Serra-Majem L, Pintó X, Basora J, Muñoz MA, Sorlí JV, Martínez JA, Fitó M, Gea A, Hernán MA, Martínez-González MA; PREDIMED Study Investigators. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Supplemented with Extra-Virgin Olive Oil or Nuts. N Engl J Med. 2018 Jun 21;378(25):e34. doi: 10.1056/NEJMoa1800389. Epub 2018 Jun 13. PMID: 29897866.

Hareer LW, Lau YY, Mole F, Reidlinger DP, O’Neill HM, Mayr HL, Greenwood H, Albarqouni L. The effectiveness of the Mediterranean Diet for primary and secondary prevention of cardiovascular disease: An umbrella review. Nutr Diet. 2025 Feb;82(1):8-41. doi: 10.1111/1747-0080.12891. Epub 2024 Aug 14. PMID: 39143663; PMCID: PMC11795232.

Isnaini N, Dewi FST, Madyaningrum E, Supriyadi. Blood pressure impact of dietary practices using the DASH method: a systematic review and meta-analysis. Clin Hypertens. 2025 Apr 1;31:e12. doi: 10.5646/ch.2025.31.e12. PMID: 40201316; PMCID: PMC11975635.

Mylavarapu M, Batra A, Garcia I, Balasubramanian A, Husnain MA, Atla RH, Muttuluru PSH, Abboud E, Silva A. Mediterranean diet versus low-fat diet on cardiovascular disease (CVD) risk factors and outcomes: A systematic review of RCTs. Medicine (Baltimore). 2026 Mar 13;105(11):e47971. doi: 10.1097/MD.0000000000047971. PMID: 41824891; PMCID: PMC12991705.

Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207. doi: 10.1056/NEJMoa0807646. Epub 2008 Nov 9. PMID: 18997196.

Yunoki K, Matsumi H, Miyoshi T, Kubo M, Hata Y, Yuasa S. Clinical Significance of Serum Omega-3 Fatty Acids on Endothelial Function in Patients with Coronary Artery Disease Under Statin Therapy. J Cardiovasc Dev Dis. 2025 Feb 5;12(2):60. doi: 10.3390/jcdd12020060. PMID: 39997494; PMCID: PMC11856868.

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This is Phase 2 of The Metabolic Rebuild. In [What If Your Blood Pressure, Cholesterol, and Fatigue Are All the Same Problem?] we discussed how scattered symptoms often belong to one cluster. Here we follow one of those clusters.

In 1985, a team of researchers set out to follow more than ten thousand British civil servants, from the senior officials in their large offices to the clerks several floors below. They would watch what happened to their health for years.

Everyone assumed they knew how it would go. The pressure sits at the top, so the senior people, the ones making the decisions and carrying the responsibility, would be the ones it wore down.

It went the other way entirely.

The further down the grades they looked, the worse the metabolic health: weight gain around the middle, higher blood sugar, blood pressure climbing, the whole cluster - known as metabolic syndrome.

And the more constant the work stress a person reported, the more likely they were to develop metabolic syndrome, in a clear dose-response way over fourteen years.

The two of them faced the same kind of working day, but not the same control over it. The higher grade civil servant carried the heavier load but could act on it; the clerk below had less on their plate yet no say over it, and it was the clerk whose health suffered more.

The harm lay not in the big, stressful day, but in the grinding, low-control load of having little say over your own day, repeated morning after morning, year after year.

You cannot breathe your way out of a load like that.

And your body knows it.

But can you switch off?

You may already know that cortisol rises when you are under pressure, and while calming practices may help lower it, the sense of being unable to entirely switch off is very common.

Cortisol is doing a job in your bloodstream regardless of how you may want to control it or how you feel about your day.

Imagine the oldest emergency your body is built to handle: a threat that means you have to run or fight. In that instant you need fuel, and you need it in your muscles and your brain straight away. Cortisol, working alongside adrenaline, is how that fuel arrives.

When cortisol rises, it instructs the liver to produce fresh glucose. The raw materials come from the body’s reserves: from muscle protein, and fat from fat stores. At the same time, cortisol instructs muscles to take up less glucose from the blood, leaving more available in the bloodstream so that it is a readily available fuel.

As a result, blood glucose climbs, and there is plenty of it, ready to be used. As it climbs, insulin rises to meet it. This is the same insulin we followed in the last article: You Lowered Your Blood Sugar. So Why Hasn’t Anything Changed?

In short bursts, high blood sugar is exactly what the body needs. The glucose is there to be burned. You run, you act, the fuel is spent, cortisol falls back, blood glucose and insulin both settle. The response ran its course and switched off.

But trouble begins when the load never lets the stress response switch off.

Two problems that keep each other running

Cortisol raises glucose, which raises insulin, which over time feeds insulin resistance. But the relationship runs both ways. Chronically high insulin drives the stress axis harder, producing what researchers call functional hypercortisolism: the system behaving as though cortisol is high without any single significant stressor.

So insulin resistance and a chronically stimulated stress response are not two problems you can treat one at a time.

Each feeds the other.

It explains something you may have experienced: you do everything right with food, and still the numbers will not move, the weight will not shift, the energy will not return because the glucose is being kept elevated from the inside.

Tired in the body, wired in the head

Cortisol is meant to move through a daily rhythm, and that rhythm is a curve: a sharp peak in the first hour after waking to get you up, then a steady fall through the day to its lowest point overnight, so the system is quiet while you sleep.

The shape of that curve depends on two things. The morning peak can only be sharp if cortisol has dropped to a real low overnight, because the rise needs a quiet baseline to climb from. And that overnight low only happens if the drive on the system eases off in the evening and lets cortisol fall.

An emotional load that never lets the stress response switch off works against both. Cortisol stays raised through the evening and into the night, so it never settles to a proper low; with the night floor lifted, the morning rise has far less room to climb. An axis kept active around the clock also tends to become less responsive over time, so the morning peak comes in blunted on top of that. The curve flattens at both ends.

You feel both ends of it. The morning peak comes in low, so getting going feels like setting off with the handbrake on. The evening level sits high, so lying down brings no wind-down.

That is the exhausted-but-wired state. The rhythm stripped of its highs and lows.

Why you wake around three

The civil servants were not losing their sleep because of one bad day. They were carrying a load that never let their stress system rest.

Overnight, blood sugar dips, more so with insulin resistance and after a late, carbohydrate-heavy meal. In a body whose cortisol should be at its lowest during the night, the system instead reaches for cortisol and adrenaline to pull glucose back up. Those are the hormones that wake you, heart going, mind switched on, around three or four.

In women in perimenopause and menopause, falling hormones add a separate thread to the same broken night: less progesterone means less of its calming compounds that relax the nervous system, so sleep becomes lighter, while low oestrogen may unsettle temperature control and bring the night sweats that wake you in the small hours.

The loop closes at night

A 2022 meta-analysis of randomised trials found that restricting sleep reduces insulin sensitivity. So a cortisol-driven bad night leaves you more insulin resistant the next day, raising insulin further, holding the stress axis in overdrive. Night and day reinforce each other.

Reading this in your own body

Insulin resistance, blood-sugar imbalances, plus early-hours waking, plus tired-yet-restless, plus weight settling around the middle, are most likely one cluster expressing through several systems, rather than four separate faults.

What to do, starting tomorrow morning

Anchor your morning with light. Get bright light into your eyes early, ideally outdoors, within an hour of waking. Ten minutes on a bright day, longer when it is grey. Morning light lifts your morning cortisol peak on purpose, and a proper high in the morning is what lets the rhythm fall again at night.

Alongside it, lower the daytime load. Remove stressors that stack up: avoid skipping meals, take a break from back-to-back demands, focus only on one thing at a time, avoid caffeine and breathe deeply. Each one eases the load.

Keep your blood sugar from running low overnight. Waking in the early morning hours often follows an overnight dip, so the aim is a good glucose supply through the night, from neither too little food nor the wrong kind. Avoid a late, refined-carbohydrate meal that spikes blood sugar and then lets it fall back sharply, and avoid going to bed on a long empty stretch after a small or early dinner. An evening meal built around protein, fat, and fibre releases its energy slowly and evenly. If you still wake up, a small protein-and-fat snack before bed, such as a little full-fat yoghurt or a few nuts, can be enough to keep the dip from happening.

You now understand why being told to relax never quite worked. Cortisol is a metabolic hormone driving your blood sugar and is locked together with insulin. Calming techniques can be helpful, but are not able by themselves resolve a metabolic stress loop that remains active underneath.

References

Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ. 2006;332(7540):521–525. doi:10.1136/bmj.38693.435301.80. PMID: 16428252.

DeFronzo RA, Auchus RJ. Cushing Syndrome, Hypercortisolism, and Glucose Homeostasis: A Review. Diabetes. 2025;74(12):2168–2178. doi:10.2337/db25-0120. PMID: 40663715.

Lengton R, Schoenmakers M, Penninx BWJH, Boon MR, van Rossum EFC. Glucocorticoids and HPA axis regulation in the stress–obesity connection: A comprehensive overview of biological, physiological and behavioural dimensions. Clinical Obesity. 2025;15(2):e12725. doi:10.1111/cob.12725. PMID: 39623561.

Sondrup N, Termannsen A-D, Eriksen JN, Hjorth MF, Færch K, Klingenberg L, Quist JS. Effects of sleep manipulation on markers of insulin sensitivity: A systematic review and meta-analysis of randomized controlled trials. Sleep Medicine Reviews. 2022;62:101594. doi:10.1016/j.smrv.2022.101594.

Robertson-Dixon I, Murphy MJ, Crewther SG, Riddell N. The Influence of Light Wavelength on Human HPA Axis Rhythms: A Systematic Review. Life (Basel). 2023;13(10):1968. doi:10.3390/life13101968. PMID: 37895351.

She brought a folder of blood tests.

Two years of them, taken every six months. Fasting glucose, normal. Her three-month blood sugar average was normal, and a little better each time. She had earned those results. The bread was gone. The walk after dinner had become routine. Her doctor had looked them over and told her to carry on exactly as she was.

And still she was sitting across from me describing the four o’clock slump, the weight that had climbed year on year since her mid-forties and would not come off however carefully she ate, a blood pressure reading that kept creeping upward, and the evening cravings she could not talk herself out of.

Normal results, every six months. And almost nothing she could feel had changed.

That contradiction is what brings most people to my door. They read it as personal failure, or as a reason to try harder. She had assumed the same.

But she had been watching the wrong number all along.

The Number Hiding Behind the One You Watch

Here is what those normal results could not show her. To keep her blood sugar in range, her body had been pouring out insulin for hours after every meal. The glucose could still read normal because insulin was working overtime behind it.

A pathologist named Joseph Kraft spent his career measuring exactly this. He tested thousands of people with glucose tolerance testing, measuring not only glucose but the insulin response required to keep glucose in range. In a large share of them, insulin was running high years before glucose ever drifted. The glucose test had pronounced them fine. Their insulin told a very different story.

That is the number my client had never had tested. And it changes what you do next.

One Mechanism Wearing Five Disguises

Last time we looked at clustering: how changing cholesterol, rising blood pressure, fatigue, stubborn weight and broken sleep are not five separate problems but one, expressed five ways.

High insulin is the thread running through all of them. It instructs the liver to make and store fat, mediating the lipid changes. It tells the kidneys to hold on to sodium, raising blood pressure. It keeps fat stores locked, so the weight will not release however carefully you eat. It keeps hunger turned up, and that explains the evening cravings.

Lower the glucose reading alone, and none of these mechanisms changes significantly.

Lower the insulin load, and all five start to unwind together.

So the real question is how to bring insulin down, not just glucose. Two levers do most of the work.

The Back Door My Client Had Already Found

She had found one of them without knowing it. The walk.

When a muscle contracts, it pulls glucose out of the blood without needing insulin at all. The contraction itself moves the glucose transporters to the cell surface. That is what her after-dinner walk was doing, and she felt it helping.

But a walk is the smallest version of this intervention. Muscle is your largest glucose sink, and it works around insulin resistance rather than against it. The more muscle you carry and use, the more glucose leaves your blood through a route that does not depend on insulin, the hormone your cells may have become less responsive to.

So here is the intervention beyond the walk: add resistance work twice or three times a week. Bodyweight counts. One walk clears a single meal. More muscle clears glucose every day, not only when you move it but at rest, where extra muscle acts as a larger store waiting to be filled.

Fewer Hours, Less Insulin

The second lever is time. Every time you eat, insulin rises. Graze from breakfast until late evening and it rarely comes all the way down. Bring your eating into a shorter daily window and you create fewer surges across the day. Recent trials of time-restricted eating show improved insulin resistance, even when weight loss is not the main driver, particularly when the eating window is earlier in the day.

The order within a meal works the same way. Vegetables and protein before the starch may blunt the insulin rise. In a trial in people with type 2 diabetes, eating vegetables and protein before the starch lowered the post-meal glucose rise by around 50% and the insulin response by around 25%, without changing anything else on the plate.

This article sits inside Phase 2 of the Metabolic Rebuild, where we look at deeper mechanisms and how they can be influenced with targeted lifestyle and nutritional interventions.

What To Do This Week

I want to emphasise the foundation. If you have not worked through Phase 1, start there: protein and fibre at every meal, refined and processed carbohydrate reduced, the right fats, sleep and stress addressed. Without that base, the steps below have less to act on.

Then go beyond the basics:

• Add two short resistance sessions this week. Build muscle as a working glucose sink.

• Bring your eating into a window, ten to maximum twelve hours to begin with, so insulin has time to fall.

• Sequence each meal: vegetables, protein and fat first, starch last. Having starch last helps to ‘crowd it out’. Eating the starchy foods when you are not starving helps with eating less of them.

Each of these lowers your insulin load. Bring down the one central driver (insulin), and the five problems it produces improve together: because they were never separate.

My client did not need to try harder. She needed to change the strategy.

In one of the next articles, I plan to go deeper into cortisol: the stress hormone locked together with insulin, and why the two keep each other running.

If you have the paid Phase 2 Clustering Guide, this is the insulin-resistance chapter. You can download the guide here:

Read more

San Francisco, 1988.

Gerald Reaven stepped up to the podium at the American Diabetes Association annual meeting. He was a Stanford endocrinologist, chosen that year to deliver the Banting Lecture, the most prestigious platform in the field.

The audience expected a talk about blood sugar.

What Reaven presented was entirely different.

For years, he had been watching something in his patients: the ones who developed type 2 diabetes were rarely presenting with elevated blood sugar alone. They also had elevated blood pressure. They had elevated triglycerides and low HDL. They had a characteristic distribution of weight around the abdomen. These findings were seen together, consistently enough that Reaven was certain they were not coincidence.

He called the cluster Syndrome X.

The X was intentional. It meant that he did not know the full mechanism connecting everything in the cluster. But he was certain of one thing: these were not separate conditions with separate causes. They were different outputs of a single underlying imbalance. He identified that imbalance as insulin resistance.

The medical community was slow to support this. For good reason: medicine was built around the diagnostic category, the single named disease with its own aetiology, its own targets, its own management pathway. The idea that high blood pressure, dyslipidaemia, impaired glucose regulation, and central adiposity were all downstream of one shared upstream process required clinicians to look backwards in a direction the framework did not map.

It would take another decade and a half before the cluster was formalised as metabolic syndrome by major international bodies. By then, the evidence was unambiguous.

The findings cluster for a reason. They are not separate problems. They are different expressions of the same underlying imbalance.

If you are in your 40s, 50s, or 60s, with elevated blood pressure, abnormal lipids, blood sugar trending upward, frequent fatigue, sleep that does not restore, persistent cravings, or weight that does not shift regardless of what you try, you are likely looking at this cluster. Taken alone, each finding leads to a partial answer. Taken together, they lead to a different one.

The Problem With Treating Each Number Separately

When several things go wrong at the same time, the mind wants to make a list. The list feels manageable. Each item gets a name, a treatment, a target.

What the list cannot do is ask: what produced all of these?

In conventional medicine, the priority is risk management: bring the cholesterol down, bring the blood pressure down, keep the blood sugar from going higher. These are rational goals, and the interventions that achieve them are often effective for what they are designed to do.

What they are not designed to do is address the terrain that produced the numbers in the first place.

That terrain is what Phase 2 of The Metabolic Rebuild is about. You have already built the foundations: food architecture, sleep, stress load, the structural fats in your cell membranes. Those foundations have to be in place. But they do not identify which mechanism is driving your specific combination of imbalances, and they do not target it directly. That is what Phase 2 does.

What Your Results Are Trying to Show You

Phase 2 introduces a different way of looking at symptoms and test results. Instead of a list, we look at a cluster.

We look for what connects them: asking whether one underlying process in the body could be producing all of them together.

In metabolic syndrome, multiple markers frequently converge on a single mechanism. Treating the markers without addressing that mechanism is the reason the underlying imbalance persists even when individual results improve.

For the majority of people in their 40s, 50s, and 60s with this combination of findings, that mechanism is insulin resistance.

One Mechanism, Five Expressions

Insulin resistance means that cells throughout the body have become less responsive to insulin. The pancreas compensates by producing more. For a time, blood sugar stays within range. But the chronically elevated insulin is doing other things, in other systems, simultaneously.

In the liver. When insulin is chronically elevated, the liver responds by producing more fat. Triglycerides rise in the bloodstream. The LDL the liver produces becomes smaller and denser, a form more likely to penetrate artery walls. HDL falls. This can occur even without an obvious change in the diet. It is driven by elevated insulin. A 2025 review in Diabetes and Metabolism Journal confirmed this as a central driver of the lipid changes seen in metabolic syndrome.

In the blood vessels. Insulin normally signals blood vessel walls to produce nitric oxide, a compound that relaxes and widens the vessels. In insulin resistance, that instruction is not reaching the cells. The vessels become less able to relax on their own. Sodium is also retained in greater amounts, when insulin is high, adding to the pressure. The result is elevated blood pressure, and in this context, it is a direct consequence of insulin resistance. A 2022 review in Frontiers in Medicine confirmed this as a core mechanism connecting insulin resistance to high blood pressure.

In the mitochondria. Mitochondria are the structures in every cell that convert food into usable energy. Chronically elevated blood sugar and low-grade inflammation generate damaging molecules that wear them down, making them less efficient. The outcome is less energy reaching the brain and muscles: fatigue that does not lift with rest, brain fog, reduced tolerance for physical effort. A 2025 review in Frontiers in Endocrinology confirmed this as a key mechanism connecting insulin resistance to these symptoms.

In sleep. Insulin resistance disrupts sleep in two main ways: blood sugar fluctuates during the night, and cortisol, the stress hormone, remains elevated into the evening when it should be falling. Both keep the nervous system too alert to settle. The relationship also runs in the opposite direction. A 2022 systematic review in Cureus confirmed that insufficient sleep significantly worsens insulin resistance. Each drives the other, and improving sleep in isolation rarely resolves either.

In appetite. Chronically elevated insulin impairs the brain’s sensitivity to leptin, the hormone that tells the brain that energy stores are adequate. When that message is blunted, the brain does not receive a clear message that the body has enough. Hunger persists. Cravings persist, particularly for rapidly absorbed carbohydrates. This is a communication issue, a result of insulin resistance. It has nothing to do with self-regulation or your willpower.

Five expressions. One mechanism connecting all of them.

Lowering the Number Is Not the Same as Fixing the Cause

A medication that lowers blood pressure acts on the blood vessel. A statin acts on cholesterol synthesis in the liver. A drug that improves blood sugar acts on glucose uptake or insulin secretion pathways. Each does what it is designed to do.

None of them addresses the upstream driver: the state of insulin resistance that produced the liver responses leading to dyslipidaemia, the vascular dysfunction, the blood sugar elevation, and the fatigue at the same time.

This is not an argument against the prescriptions. For many people, a statin or an antihypertensive is both appropriate and necessary. The cardiovascular risk is real and the medication addresses it. However, it does not address the insulin resistance running underneath, as that is not what it was designed for.

The point is that medication and clinical nutrition work on different targets. One manages a marker out of range. The other works on the mechanisms producing it. Both are needed. Neither replaces the other.

Phase 2 adds the reasoning layer: understanding which mechanisms are driving your specific combination of imbalances, and what nutritional and lifestyle interventions may act on and influence those mechanisms directly.

The Next Layer: Finding the Driver

If you have completed Phase 1 steps, you’ve already collected your data. You documented your symptoms, your diagnosed conditions, your test results. You worked on that in Phase 1 and now we are moving to Phase 2.

Begin looking at your data as a cluster.

Take the symptoms and markers you recorded. Which ones are showing up: your energy, your sleep, your blood tests, your weight? Which ones have not improved despite getting the basics right? (If you haven’t yet completed Phase 1 with the basics of the step-by-step guide, you may want to start there)

Many of them are closely related, with one process underneath driving them. For many people among my readers, a main process at the centre is insulin resistance.

How to Recognise This Cluster in Yourself

First, check if this sounds like you: Energy that drops sharply an hour or two after eating, and a pull toward something sweet or starchy soon after. Weight that has gathered around your middle regardless of what you change. Irritability when a meal runs late. On your blood results, triglycerides on the high side, HDL on the low side, fasting blood sugar at the top of the normal range or just above it.

If this is you, insulin resistance is likely at the centre of your cluster. Here is your next step.

Make sure the groundwork we discussed in Phase 1 is in place first: protein and fibre at every meal, refined and processed carbohydrate reduced, the right fats on your plate.

With that in place, the recommendation here is to walk for fifteen minutes after your largest meal of the day. Not anytime in the day. After a main meal, and ideally after the largest meal.

When a muscle contracts, it pulls glucose out of the bloodstream through a route that does not require insulin at all. The glucose from your meal is cleared with less insulin behind it. You are giving the body a second way to handle the same meal, one that bypasses the exact mechanism that has become impaired. Done consistently after meals, this lowers the total insulin load your body works under, and lower insulin is what begins to loosen the liver, the blood vessels, the appetite, and the fatigue at once, because each was responding to that same elevated insulin.

It costs you fifteen minutes and no change to what you eat.

What If Insulin Is Not the Whole Story?

Beyond insulin resistance, which is a common cluster, there are others. Your own combination may centre on stress and cortisol, gut function, sex hormones, or thyroid function. Each has its own set of characteristics. In the clustering guide below, I explain these clusters, how to spot them, and the next steps for working with each one.

The Clustering Guide: Identify Yours

I built the Clustering Guide around the clinical framework I use when working with my clients one-to-one: the same process of reading symptoms and findings as a pattern. Each cluster is described in terms of your lived experience: what it feels like day to day, which symptoms tend to travel together, what your blood tests may be showing. Read through the guide to identify which ones are relevant to you right now. Then follow the guidance on what to do about it.

Read more

Your blood test results are real data.

Processed by a certified laboratory, measured against established reference ranges, reviewed by a trained clinician.

Every number on that page reflects something that was genuinely happening in your body on the day the sample was taken.

The flags are real too.

A high result is high. A borderline is a borderline. The reference ranges exist for good reason.

But here is what none of that tells you:

You may have influenced those numbers this morning.
You may have influenced them yesterday.
And you have almost certainly been influencing them over time: through meals, sleep, movement, stress, medication, and recovery.

Your blood results show what changed. They do not show what was changing them.

Most people receive their results and wait to understand what to do next. That makes sense. The results look like a report from an authority, something handed to you, about you, by someone who knows more than you do.

But those numbers do not describe someone else’s territory. They describe your liver, your pancreas, your cardiovascular system, your biochemistry. And the person making the most consequential daily decisions about that biochemistry, what to eat, when to sleep, how much to move, what to prioritise, is you.

You were never a spectator. You were always the main player.

The only thing missing was the understanding of what those decisions were actually doing.

For some people, the reality is more complex. Genetics, long-standing hormonal changes, years of metabolic imbalance already underway, conditions that played a significant role before any decision could have made a difference. For some, those forces are still active. None of that is the result of choices made or not made.

However, our daily decisions from this point forward are among the most powerful levers available. Every meal influences your triglycerides, your fasting glucose, your insulin response. Every month of unaddressed metabolic imbalance shows up, eventually, in the same numbers.

The results on your last panel are not fixed or inevitable. With the right information, they can be modified.

This guide is designed to help you stop reading your results as isolated numbers and start seeing them together.

That is the gap this guide closes. That is the missing variable:

The understanding that should have come with your results. What each marker is actually measuring, what drives it, and what the pattern across all of them is telling you as a whole that no single flagged number can.

It is impossible to make the right decisions about something you do not understand. And you are already making them. Learn to read the whole picture:

Download the guide here: “What Your Blood Tests Are Actually Telling You” . This is the clinical guide most blood test appointments never provide.

Next week, I will take this one step further.

A statin lowers cholesterol. An antihypertensive lowers blood pressure. These medicines work through known mechanisms and produce measurable results.

But each one is prescribed to target a specific part of the picture.

The daily decisions that affect your health as a whole do not stop when a prescription starts. Understanding your markers means knowing exactly what the prescription can and cannot do, and what remains in your hands.

Feel free to leave a comment on this post and let me know what you’d like to learn more about. I am all ears and genuinely interested in hearing what you need right now. What you share helps me see any additional support, clarification, and companion pieces that may be needed alongside this guidance.

It usually starts with a line on a blood test.

LDL: high.
Total cholesterol: high.
A little red flag beside the result.

And suddenly, one molecule that the body depends on begins to look like the enemy.

Cholesterol is not inherently harmful. On the contrary, it is biologically important, a key substance for normal function, produced mostly in the liver, and also in smaller amounts in other tissues. We need it to build cell membranes, produce hormones such as oestrogen, testosterone and cortisol, make bile acids for fat digestion, and support vitamin D production. Without cholesterol, cells would lose their structure, hormones would not be made, and digestion would suffer.

Cholesterol travels in transport particles

Cholesterol is lipophilic: more like oil than water, so it cannot move freely through the watery bloodstream. The body therefore packages cholesterol and triglycerides into lipoproteins these are able to move in the bloodstream; they are the transport particles we measure as LDL, HDL, VLDL and others.

LDL carries cholesterol from the liver towards tissues. HDL helps carry excess cholesterol back towards the liver for processing. VLDL carries triglycerides, a form of stored energy made from dietary fat and excess carbohydrate. As VLDL unloads triglycerides, it transforms into smaller particles, including LDL.

So labelling LDL as “bad” and HDL as “good” is too simplistic and leads to misunderstanding.

LDL is not “bad” by design. It is part of the body’s lipid transport system. However, when too much of it, specifically too many ApoB-containing particles, including LDL, VLDL remnants and Lp(a), remain in circulation for too long, it can become problematic, especially when the artery wall is more vulnerable because of inflammation, insulin resistance, high blood pressure, smoking or oxidative stress. Under those conditions, ApoB-containing particles can enter the artery wall, become retained and modified, and contribute to plaque formation.

Triglycerides: stored energy in circulation

Another measured marker in your test is fasting triglycerides (TG). Triglycerides are the body’s main storage form of fat. After a meal, they are transported to be used as an energy source. Between meals, they can be released from fat tissue and used as fuel.

High fasting triglycerides often suggest the body is struggling to handle energy well: either the liver is sending out more VLDL particles, which carry triglycerides through the blood, or that the body is not clearing these VLDL particles efficiently.

Too much refined carbohydrate, alcohol, visceral fat, insulin resistance, poor sleep and low activity increase the liver’s supply of fatty acids, so the liver increases its triglyceride production. High triglycerides reflect increased triglyceride-rich VLDL particles (or reduced clearance of VLDL particles). That affects HDL and LDL: HDL may fall, a pattern we commonly see in metabolic dysfunction.

Cholesterol changes through life

Cholesterol is dynamic. It can shift with age, weight change, thyroid function, menopause in women, illness, stress, diet and medication.

Ageing can affect cholesterol, and blood cholesterol tends to rise over time. There is an idea circulating that an ageing brain needs more cholesterol. I could not find any evidence of that.

The brain contains a large amount of cholesterol, around 25% of the body’s cholesterol, and cholesterol is essential for myelin, synapses and normal brain function. But brain cholesterol is largely made inside the brain itself. Circulating LDL cholesterol in the blood does not generally cross into the brain to supply it, because the blood–brain barrier tightly separates brain cholesterol from peripheral cholesterol.

So the argument “cholesterol rises as we age because the brain needs more” is not supported by evidence.

A more likely explanation is that blood cholesterol often rises with age because the body becomes less efficient at clearing LDL particles from circulation. Human metabolic studies show that age-related LDL increase is explained mainly by reduced LDL removal, likely through reduced liver LDL receptor activity.

In women, menopause adds another layer. LDL, total cholesterol, triglycerides and Lp(a) often rise during late perimenopause and postmenopause, partly because oestrogen influences lipid metabolism and LDL clearance.

Men also see similar lipid changes with ageing, insulin resistance, weight gain, alcohol intake and reduced muscle activity.

Diet can shift cholesterol in different directions. Saturated fat (from sources like animal fat and butter) may raise LDL in many people. Weight loss can temporarily raise cholesterol as fat is mobilised.

Very low-carbohydrate diets that are high in protein and fat can sharply raise LDL in some lean, metabolically healthy people, the so-called “lean mass hyper-responder” pattern. A 2024 study of lean mass hyper-responders found there was not greater coronary plaque burden compared with matched controls, while triglycerides fell and HDL increased, suggesting a different metabolic context.

A high LDL in those individuals does not carry the same risk as high LDL in someone who also has high triglycerides, insulin resistance, fatty liver, hypertension and inflammation. This demonstrates that cholesterol numbers need context, and that interpretation requires looking at the wider picture.

Cholesterol still deserves attention

Your doctor tests for cholesterol because long-term exposure to LDL and other ApoB-containing particles is strongly linked to atherosclerotic cardiovascular disease. More recent research has strengthened the case for looking beyond LDL cholesterol alone: several 2024–2025 analyses show that when LDL-C and ApoB disagree, cardiovascular risk often follows ApoB more closely, because ApoB better reflects the number of atherogenic particles in circulation.

Statins are commonly recommended because they reduce cholesterol production in the liver, increase LDL receptor activity, lower LDL cholesterol and ApoB-containing particles, and have been shown in large trials to reduce cardiovascular events in people whose risk is high enough. But this does not mean every raised cholesterol result automatically requires a statin. Some people experience side effects, most commonly muscle symptoms, and statins can slightly increase the risk of type 2 diabetes in susceptible people.

Treatment with statins is a complex medical decision that should take into account the whole picture: your overall cardiovascular risk, previous cardiovascular disease, diabetes, family history, blood pressure, existing plaque, metabolic health, smoking, age, other relevant markers, possible side effects, and your own preferences after you have been properly informed. It should be a shared decision between you and your doctor, made after understanding both the potential benefits and the trade-offs.

As a clinical nutritionist, I do not see statins as a substitute for correcting the conditions that pushed risk upward in the first place. They may reduce particle burden, but they do not replace the work of improving insulin resistance, blood pressure, inflammation, body composition, diet quality, sleep and physical activity.

Existing plaque changes the conversation. Once plaque is present, especially if coronary artery calcium (CAC) or CT imaging shows significant burden, the question is no longer theoretical. Plaque burden is one of the strongest predictors of future cardiovascular events, and current guidelines increasingly use CAC and imaging to clarify risk. So the more evidence there is that atherosclerosis has already begun, the more seriously particle-lowering and risk-reduction need to be considered.

At this point, the question is no longer whether cholesterol deserves attention. It does.
The more important question is: what does your cholesterol mean when you look at the whole picture?
That is where most interpretation goes wrong and misses the point.

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In February 1971, two Danish scientists stepped off a supply plane onto the frozen west coast of Greenland carrying centrifuge instruments, medical equipment, and a question nobody could answer.

The wind cut across the ice hard enough to sting the face. Hunting boats sat pulled onto the snow beside wooden houses painted red and blue against the white landscape. Inside one home, seal meat simmered slowly in a pot while strips of Arctic char dried beside a window filmed with frost.

To the visiting researchers, one thing seemed obvious:

The people living here should have been dying of heart disease.

The Population That Challenged Understanding

At the time, much of Western medicine believed fat itself was the enemy. Saturated fat. Animal fat. Marine fat. It barely mattered. The prevailing logic was: the more fat a population ate, the more blocked arteries and fatal heart attacks they should develop.

And yet, the blood samples coming back from Inuit hunters told a different story.

Their triglyceride levels were unexpectedly low. Their blood appeared less prone to clot than expected. Diabetes was extremely rare and reports of fatal heart attacks seemed lower than researchers expected from a population eating such large amounts of fat.

One of the researchers, Hans Olaf Bang, later became fixated on the contradiction.

How could men eating seal, whale blubber, and fatty fish through long Arctic winters show patterns that medicine associated with lower cardiovascular risk?

At first, scientists searched for familiar explanations.

Maybe it was the cold.

Maybe it was genetics.

Maybe hauling hunting equipment across ice floes changed metabolism in ways modern life did not.

The Clue Was in the Blood

But the clue revealed itself in their blood.

Inuit blood contained unusually high levels of marine omega-3 fats. And when researchers later gave marine oils to people far from Greenland, some of the same changes appeared: lower triglycerides, less clotting, and lower levels of inflammation.

The cold had not travelled with them.
Their genes had not changed.

The dietary fat had.

Fish oil.

Seal oil.

Marine fat.

In some Arctic communities, seal oil was treated almost like a form of wealth. Elders described it not merely as food, but as strength, warmth, endurance. Hunters carried it through winters because it sustained life where little else could. Children were given it deliberately.

Long before laboratories gave these fats scientific names, people living close to the sea already understood something modern nutrition had forgotten:

some fats nourished differently than others.

Fats That Become You

Decades later, researchers would identify the key compounds within these foods: omega-3 fatty acids, particularly EPA and DHA.

But the important detail is what these fats actually do inside the body.

They become part of the body itself.

Every cell in the body is wrapped in a membrane. Blood cells. Immune cells. Heart tissue. Blood vessels. Brain tissue. And the fats embedded in those membranes influence how flexible they remain, how inflammatory signals are handled, how blood vessels respond under stress, and how easily blood tends to clot.

The Modern Fat Imbalance

Omega-3-rich marine foods gradually disappeared from many modern diets over the past century, while another category of fat expanded dramatically.

Industrial seed oils.

Soybean oil. Corn oil. Sunflower oil. Cottonseed oil.

These oils became cheap, shelf-stable, and profitable to produce at massive scale. They entered processed foods, restaurant fryers, packaged snacks, bottled dressings, bread, even foods marketed as “healthy.”

Before industrialisation, humans consumed these oils in relatively small amounts because extracting them required substantial mechanical processing. But by the late twentieth century, they had become one of the dominant calorie sources in many Western diets.

Omega-6 fats are not inherently “bad.” In fact, they are needed in a balanced diet.

The problem is proportion.

Marine omega-3 fats and omega-6 fats compete for many of the same biochemical pathways involved in inflammation and cellular signalling. Historically, human diets contained these fats in a far more balanced relationship. Modern diets shifted heavily toward omega-6 while simultaneously reducing omega-3 intake.

The result was:

Cell membranes built from different materials.

Inflammation Needs an Off Switch

These cell membranes behave more like control panels and the fats embedded in them are crucial.

Imagine inflammation as the body’s fire response system.

You need it.

Without inflammation, wounds would not heal and infections could become fatal.

Inflammation is required in injury and illness, but it can be harmful if it is permanently activated.

Omega-6 fats and omega-3 fats both participate in inflammation, but they tend to push it in different directions.

Omega-6 fats are not inflammatory by default. However, if the diet is dominated by omega-6-rich oils and is low in marine omega-3 fats, the balance of lipid signals involved in inflammation and resolution may shift. Arachidonic acid, an omega-6 fat stored in cell membranes, can be converted into inflammation signalling molecules.

Omega-3 fats help create signalling compounds that are generally anti-inflammatory and, importantly, help switch inflammation off once the danger has passed.

The proportion problem may make inflammatory pathways easier to activate and harder to resolve.

The Injury Beneath the Surface

And downstream, several things begin happening simultaneously.

Over time, inflammation creates the kind of environment where arterial injury becomes more likely to persist.

Arteries are living tissue lined by an extraordinarily delicate inner layer called the endothelium.

When inflammation repeatedly irritates that lining, the body responds like it would to a wound.

Immune cells move in.

Cholesterol particles become trapped more easily inside damaged areas.

Plaques begin forming beneath the vessel surface.

And if inflammation remains chronically active, those plaques become more unstable and dangerous over time.

At the same time, blood vessels under inflammatory stress lose their flexibility to relax properly.

Pressure inside the system rises.

The heart must push harder.

Blood pressure gradually increases.

The Cardiovascular Case for Marine Fats

Following this discovery, omega-3 fats became central in cardiovascular research, as they appeared to influence multiple layers of cardiovascular biology simultaneously:

• Inflammation. They appeared to reduce inflammation through anti-inflammatory signals between cells.

• Triglycerides. They lowered triglycerides by directly affecting triglyceride synthesis in the liver.

• Blood vessel flexibility. They appeared to improve the function of inner membranes of vessels and maintain arterial elasticity.

• Blood clotting. They appeared to reduce clotting tendency.

• Heart rhythm stability. They appeared to improve cardiac electrical activity and reduce arrhythmia risk.

• Cell membrane function itself. They became incorporated into cell membranes, altering membrane fluidity, signalling, and receptor function.

Researchers later described omega-3 fats as structural information for the body.

So the old Arctic observations now looked entirely different.

Inuit bodies were being built, day after day, from different raw materials.

The Body’s Own Calm-Down Signals

More importantly, modern research has further transformed the omega-3 story.

Scientists now know omega-3 fats are used to create specialised molecules called resolvins, protectins, and maresins. These are compounds some researchers describe as the body’s own “resolution signals.”

This new discovery changed our scientific understanding as for years, inflammation research focused mostly on what starts inflammation. Now scientists are increasingly studying what resolves it.

The Imbalance You Cannot Feel

Omega 6 fats are incorporated into many processed foods. You do not feel the changes happening in real time.

There is no alarm bell when membrane composition changes.

No symptom that inflammation becomes easier to trigger.

Which is partly why cardiovascular disease can appear to arrive suddenly after decades of such changes underneath the surface.

Annual check-ups usually miss the beginning of this imbalance. They rarely assess the fatty-acid composition of cell membranes directly through markers such as the Omega-3 Index, which reflects how much EPA and DHA have been incorporated into red blood cell membranes over time.

By the time blood pressure rises significantly, plaques become visible on a CT scan, or glucose regulation deteriorates, the biological functions producing those changes may already have been developing for years.

But don’t believe for one minute that a single nutrient can prevent disease on its own. A nutrient doesn’t work in isolation. Still, it can play a central role within a balanced diet, and without enough of it, the whole system may start to suffer.

The Arctic findings exposed something medicine had oversimplified:

Not all fats behave the same inside the body.

Some are burned to produce energy.

Some are stored and become the building blocks of the body. The quality of the blocks is key.

These fats become structural material for the systems regulating inflammation, circulation, and resilience itself.

Phase 1: Bring Marine Foods Back In

In Phase 1, the emphasis is on rebuilding the diet around foods modern eating patterns have pushed aside. Aim to include oily fish or shellfish at least 3 times throughout the week, incorporating them into the diet consistently rather than only occasionally. Good options include:

• Sardines packed in olive oil.

• Mackerel served with herbs, lemon, and a bitter green salad.

• Anchovies used as a savoury seasoning in dressings, sauces, or vegetable dishes.

• Salmon roasted with lemon and herbs.

• Mussels steamed with garlic and parsley.

The lesson from Greenland was that the body changes according to what it is consistently built from.

Some of the earliest stages of disease begin when something harmful enters the diet or when something ancient disappears from it.

Feel free to leave a comment on this post and let me know what you’d like to learn more about. I’m all ears and genuinely interested in hearing what you need right now. What you share helps me see any additional support, clarification, and companion pieces that may be needed alongside this guidance.

References

Ayee MAA, Bunker BC, De Groot JL. Membrane modulatory effects of omega-3 fatty acids: Analysis of molecular level interactions. Curr Top Membr. 2020;86:57-81. doi: 10.1016/bs.ctm.2020.08.001. Epub 2020 Sep 14. PMID: 33837698.

Bang HO, Dyerberg J, Nielsen AB. Plasma lipid and lipoprotein pattern in Greenlandic West-coast Eskimos. Lancet. 1971 Jun 5;1(7710):1143-5. doi: 10.1016/s0140-6736(71)91658-8. PMID: 4102857.

Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011 May;93(5):950-62. doi: 10.3945/ajcn.110.006643. Epub 2011 Mar 2. PMID: 21367944; PMCID: PMC3076650.

Daly K, O’Sullivan K, O’Sullivan TP. Major structure-activity relationships of resolvins, protectins, maresins and their analogues. Future Med Chem. 2022 Dec;14(24):1943-1960. doi: 10.4155/fmc-2022-0206. Epub 2022 Nov 30. PMID: 36449363.

Dyerberg J, Bang HO. Haemostatic function and platelet polyunsaturated fatty acids in Eskimos. Lancet. 1979 Sep 1;2(8140):433-5. doi: 10.1016/s0140-6736(79)91490-9. PMID: 89498.

Golanski J, Szymanska P, Rozalski M. Effects of Omega-3 Polyunsaturated Fatty Acids and Their Metabolites on Haemostasis-Current Perspectives in Cardiovascular Disease. Int J Mol Sci. 2021 Feb 27;22(5):2394. doi: 10.3390/ijms22052394. PMID: 33673634; PMCID: PMC7957531.

Kjaergaard M, Andersen S, Holten M, Mulvad G, Kjaergaard JJ. Low occurrence of ischemic heart disease among Inuit around 1963 suggested from ECG among 1851 East Greenland Inuit. Atherosclerosis. 2009 Apr;203(2):599-603. doi: 10.1016/j.atherosclerosis.2008.07.027. Epub 2008 Aug 5. PMID: 18774134.

Lai HTM, Ryder NA, Tintle NL, Jackson KH, Kris-Etherton PM, Harris WS. Red Blood Cell Omega-6 Fatty Acids and Biomarkers of Inflammation in the Framingham Offspring Study. Nutrients. 2025 Jun 22;17(13):2076. doi: 10.3390/nu17132076. PMID: 40647182; PMCID: PMC12251348.

Surette ME. The science behind dietary omega-3 fatty acids. CMAJ. 2008 Jan 15;178(2):177-80. doi: 10.1503/cmaj.071356. PMID: 18195292; PMCID: PMC2174995.

Zehr KR, Walker MK. Omega-3 polyunsaturated fatty acids improve endothelial function in humans at risk for atherosclerosis: A review. Prostaglandins Other Lipid Mediat. 2018 Jan;134:131-140. doi: 10.1016/j.prostaglandins.2017.07.005. Epub 2017 Aug 9. PMID: 28802571; PMCID: PMC5803420.

Dear Reader,

There are evenings when the desire for dessert is not really about sugar. It is about wanting the meal to feel complete. Something cold from the fridge. Something dark, creamy, and sweet enough to feel like care rather than compromise.

That is where this Black Forest Chia Pudding works. Dessert does not have to sit outside a heart-healthy food plan. On the contrary, done well, it should satisfy the senses while supporting the functions we are trying to restore: blood sugar regulation, gut function, cardiovascular resilience, and metabolic flexibility.

Today I thought I would do something different and give you a satisfying yet health-supporting dessert.

Before we get to the spoon, let’s look at what this bowl is doing for you.

This Black Forest Chia Pudding supports health because of how it is structured. It is balanced. Per serving, it provides approximately 297 calories, 14.7g fat, 37g carbohydrate, 14g fibre, and 10g protein. That fibre-protein-fat combination changes how it behaves in the body.

Chia seeds

Chia seeds provide fibre and plant-based omega-3 fats. Their fibre slows glucose absorption, supports bowel regularity, and feeds the gut environment in a way that can help reduce low-grade inflammation and support insulin sensitivity.

Chia’s fibre forms a gel in the gut, slowing digestion and helping blunt a sharp glucose rise after eating. It also feeds gut microbes, which produce short-chain fatty acids: These compounds help restore the gut’s integrity, and regulate the immune system.

The gel-like fibre in chia (soluble fibre) also supports cholesterol reduction. It can bind bile acids in the intestine and help with their excretion. Because bile acids are made from cholesterol, the liver then uses more cholesterol to replace them, which helps lower circulating LDL cholesterol over time. The effect is usually modest, but meaningful when fibre intake is consistent and part of an overall heart-supportive diet.

Greek yogurt

Yogurt in general, but especially Greek yogurt adds protein, which improves satiety and helps regulate the glucose response of the meal by slowing stomach emptying and stimulating satiety hormones. Protein also supports insulin release in a measured way, helping glucose move from the bloodstream into cells more efficiently after eating.

Yogurt also brings fermented food into the equation. During fermentation, bacteria transform milk sugars and proteins into compounds that can be easier to digest and may support beneficial microbial activity.

Live cultures in the yogurt are beneficial bacteria that can interact with the gut microbiome, support the gut’s microbial diversity, and help maintain the gut barrier. Improving the gut barrier is important because it helps reduce intestinal permeability — often referred to as “leaky gut.” A healthier, less permeable barrier lowers the chance of harmful compounds passing from the gut into circulation, where they may contribute to inflammation.

So the point is not only how many calories or carbohydrates a dessert contains. It is also the structure of the food: the protein, fibre, fat, fermentation, and how these elements influence digestion, glucose absorption, satiety, gut signalling, and inflammation.

Cocoa powder and cocoa nibs

Cocoa brings polyphenols: compounds that may support vascular function and cardio-metabolic health by supporting blood vessel relaxation, reducing oxidative stress, and helping protect LDL particles from oxidative damage.

But it also brings something just as important: pleasure. The bitterness, depth, and richness give this dessert its satisfaction. Emotional satiety is essential. When a dessert tastes complete: creamy, dark, lightly sweet, with something to bite into, the mind is less likely to keep asking, “What else?”

Psychologically, this makes a difference because restriction often increases preoccupation with food. A dessert that feels rich and satisfying can reduce the sense of deprivation, helping the body register that the meal is complete.

Cherries

Cherries provide sweetness, colour, and their own polyphenols. Polyphenols act as protective plant compounds: in addition to the benefits I mentioned above, they too interact with gut microbes in two important ways: Gut microbes break polyphenols into smaller compounds the body can use as antioxidants, while polyphenols also help encourage the growth of beneficial bacteria. Together, these properties support a healthier gut and lower inflammation.

Cherries make the pudding feel indulgent and reduce the need for added sugar.

An important principle to keep in mind is: enjoyment and metabolic stability should not be treated as opposites.

Almond milk and a touch of maple syrup

Unsweetened almond milk keeps the base light, while a small amount of maple syrup gives enough sweetness to make the dessert enjoyable without turning it into a sugar-heavy option.

Recipe: Black Forest Chia Pudding

Serves: 2
Prep time: 15 minutes, plus overnight chilling

Ingredients

⅓ cup chia seeds
2 tbsp cocoa powder
1¼ cups unsweetened almond milk
1 tbsp maple syrup
½ cup plain Greek yogurt
½ cup pitted cherries
1 tbsp cocoa nibs

Method

Whisk together the chia seeds, cocoa powder, almond milk, and maple syrup. Divide into two containers and refrigerate overnight, until thickened.

To serve, top each portion with ¼ cup Greek yogurt, ¼ cup cherries, and ½ tablespoon cocoa nibs.

You finish the bowl with the sense that nothing has been taken away.

The pleasure is still there.

The sweetness is still there.

But the structure of the dessert is different: fibre, protein, fat, polyphenols, and enough sweetness to satisfy without the crash.

Special thanks to Julie Harrington who contributed to this recipe.

Feel free to leave a comment on this post and let me know what you’d like to learn more about. I’m all ears and genuinely interested in hearing what you need right now. What you share helps me see any additional support, clarification, and companion pieces that may be needed alongside this guidance.

Find below the complete printable recipe card + nutrition facts for paid members: save, print, and make it this week.

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Dear Reader,

Overeating sounds like something you would notice. In reality, it is surprisingly invisible.

Our modern food environment makes overeating hard to recognise. Food is engineered to be easy to over-consume, partly by increasing hedonic reward: the pleasure-driven desire to keep eating even when the body does not physiologically need more energy. As a result, our perception of intake is often unreliable.

So how do you actually know whether you are overeating, rather than just eating enough?

Start by assessing outcomes. Perception alone is not reliable

The most reliable indicator of repeated overeating is not hunger, fullness, or even calorie tracking.

It’s this:

• Your body weight tends to rise over weeks or months

• Your waist circumference tends to increase

That combination strongly suggests a sustained energy surplus, especially when the pattern persists across several weeks and measurements are taken consistently.

By measuring your waist, you can distinguish actual fat gain from short-term body weight fluctuations like water retention or glycogen shifts. Glycogen shifts are one reason water retention occurs.

Glycogen is the storage form of carbohydrate in muscle and liver, and it is stored together with water because glycogen binds water. So when glycogen stores rise, body weight can increase quickly because more water is being held with that glycogen. When glycogen stores fall, the opposite happens. This is one reason body weight can change from day to day without reflecting true fat gain or fat loss. This is often referred to as “water retention.” Water retention can also be influenced by sodium (salt) intake, hormones, stress, inflammation, poor sleep, medications, and the menstrual cycle.

To get a reliable waist measurement, use the same conditions each time: before meals, ideally at the same time of day, and not when you feel bloated.

What is driving weight gain?

Research has found that certain eating behaviours consistently increase energy intake. Some are obvious; others are much more subtle. Consider if the following are relevant to you:

• You eat when you are bored, emotional, or because food is appealing even though you are not physically hungry

• You start your meal hungry but continue eating even after reaching fullness

• You clear your plate because you don’t want to waste food, or you finish large portions simply because they are there

• You frequently snack between meals

• You eat quickly or while distracted. Satiety signals from the gut and brain take time to register, so eating rapidly makes it easier to consume more before your body recognises fullness.

• You regularly eat highly palatable, easy-to-overeat foods. These foods are typically energy-dense, often addictive and engineered to maximise reward and repeat consumption, making passive overconsumption much more likely.

• You drink calories without realising it. Such as alcohol, sugary drinks, or specialty coffees. Liquid calories are particularly tricky because your body registers them less effectively for fullness compared to solid foods. As a result, you may consume these calories in addition to your normal food intake, rather than compensating by eating less solid food. Alcohol can also make it easier to eat more than you planned by lowering inhibition and making tempting foods harder to resist.

Controlled feeding studies have shown that ultra-processed diets can increase spontaneous calorie intake by hundreds of calories per day, even when researchers attempted to match the diets for nutrients such as fat, carbohydrate, sugar, fibre, and protein. In practice, participants still ended up eating significantly more food overall when the foods were ultra-processed.

And “ultra-processed” does not only mean obvious junk food. It can include many foods that appear “healthy”: breakfast cereals, flavoured yoghurts, protein bars, packaged breads, ready-made sauces, plant-based meat alternatives, low-fat snacks, diet products, meal-replacement shakes, and many “high-protein” or “low-fat” packaged foods. The common features are that the food comes in a package, has been heavily processed, and has been industrially formulated to be convenient, highly palatable, easy to prepare, and quick to eat. In other words, you may be eating more ultra-processed food than you realise.

The point is this: you rarely consciously decide to overeat. The environment and circumstances often do most of the work.

What about “reasonable portions”?

You might often wonder whether you are eating more than you should, and even feel guilt or shame about it.

However, you may decide to be kinder to yourself if you recognise that we are naturally programmed to seek out and consume calorie-dense food whenever it is available. For most of human history, food was scarce or unpredictable. This was a wise adaptation in that context, but it clashes with today’s environment of food abundance and convenience.

This mismatch between ancient biology and modern food availability makes it very easy to underestimate intake, especially with:

• snacks

• liquid calories

• energy-dense foods.

By energy-dense foods, I mean those that contain a lot of calories in a relatively small amount. For example, a meal with few vegetables or other high-volume foods, and a larger proportion of calorie-dense foods such as oils, cheese, nuts, fatty meats, creamy sauces, pasta, rice, bread or large portions of starchy foods. These foods, when they dominate the plate, can shift the meal towards a higher calorie load.

Building systems for success

You cannot reprogram your biology, but you can certainly build systems around it: by increasing awareness and by presetting your choices and your environment.

This may include smaller portions, balancing your meals, avoiding keeping highly tempting foods constantly available at home, planning meals ahead of time, slowing down eating, reducing distracted eating, and creating routines that make the easier choice the healthier one. Systems are more reliable than willpower alone.

Now you have a better idea on how to answer the question:

“Do I repeatedly eat beyond hunger or beyond the amount my body actually needs?”

It is more reliable to find the answer by using observable criteria. To summarise the thought process, I have included a flowchart below. Run it, reflect on it, and let me know what comes up for you.

Factors beyond overeating

As you can see in the flowchart, you may want to consider other contributing factors to weight gain. So if any of these are present, it is worth addressing them one by one:

• You may have added or changed your medication recently. Some medications can increase appetite, alter metabolism, promote fluid retention, or reduce energy and motivation, indirectly contributing to weight gain.

• You may have recently reduced your physical activity while your energy intake has stayed the same. In that case, the same amount of food may now exceed your current energy needs.

• Your body may be retaining fluid. This can be the result of stress, hormonal changes, high sodium (salt) intake, inflammation, poor sleep, or medications as mentioned above. This may increase body weight without necessarily reflecting fat gain.

• You may be in perimenopause or menopause, when hormonal changes can influence appetite, sleep, energy expenditure, fat distribution, and weight gain. Hormonal changes are often responsible for making weight gain easier even without obvious dietary changes.

• You are gaining muscle mass through training. Muscle gain itself can increase body weight even when body fat is not increasing.

These factors can influence body weight independently of energy intake through mechanisms such as altered water balance, hormonal regulation, energy expenditure, appetite signalling, or changes in body composition.

That said, I must highlight that weight gain in some cases is not problematic and is in fact beneficial. For example, if body weight increases because you are gaining muscle through resistance training, while waist circumference remains stable or decreases, that is a very different pattern from gaining abdominal fat.

The ultimate goal is not the lowest possible number on the scale, but a healthier body composition: more or better-preserved muscle, less excess abdominal fat, and improvements in the markers that reflect metabolic and cardiovascular health.

This is why waist circumference should be measured. It gives you more clarity about changes in abdominal fat than body weight alone, especially when muscle gain, training adaptations, or glycogen-related water changes are also influencing the scale.

Crucially, though, this doesn’t invalidate behavioural patterns that may still need correcting. I just want to stress there’s often more complexity involved.

Having said that, there is one important exception: you may already be carrying more abdominal fat than is metabolically healthy, without seeing changes in your waist or body weight. In this case, your intake may simply be matching the energy needs of your current body size.

But stability is not the same as metabolic health. If your body composition, blood pressure, glucose, insulin, triglycerides, or other markers suggest excess risk, it is more useful to ask: “Am I maintaining a metabolic state my body would benefit from improving?”

One overlooked factor: loss of control

So far, we have looked at overeating through outcomes: weight, waist, and body composition. But there is one more important angle that should be considered: your sense of control around food.

If eating often involves feeling unable to stop, episodes of loss of control, or guilt and shame afterwards, it may point to a more complicated relationship with food.

In that case, the answer may not be more discipline or another strategy, but a different kind of support. A specialist in eating behaviour can help identify what is driving the pattern and help you address it with care.

Putting it all together

So use the flowchart to answer the question: “Am I overeating?” Work through it from top to bottom to see whether overeating is likely, or whether another explanation may be contributing to the change.

Answer each question honestly based on your patterns over the past 4 weeks. The result should help you distinguish between likely overeating, and situations where extra support might be needed.

Overeating is rarely obvious in the moment.

It is a pattern and behaviour that has to be recognised. And what can be recognised can often be changed.

The most reliable way to recognise it is by asking:

“Is my weight or waist increasing, and if so: do my eating patterns make that increase likely?”

Feel free to leave a comment on this post and let me know what you’d like to learn more about. I’m all ears and genuinely interested in hearing what you need right now. What you share helps me see any additional support, clarification, and companion pieces that may be needed alongside this guidance.

References

1. Burr EK, Dvorak RD, de Leon AN, Klaver SJ, Peterson R, Hayden ER, et al. Understanding Loss of Control Eating Through the Lens of Expectancies and Reinforcement Sensitization. Psychiatry. 2024;88(1):55. doi:10.1080/00332747.2024.2403664 PubMed PMID: 39466974.

2. Santos-Báez LS, Ravelli MN, Díaz-Rizzolo DA, Popp CJ, Gallagher D, Cheng B, et al. Dietary misreporting: a comparative study of recalls vs energy expenditure and energy intake by doubly-labeled water in older adults with overweight or obesity. BMC Med Res Methodol. 2025 Dec 1;25(1). doi:10.1186/S12874-025-02568-4 PubMed PMID: 40287632.

3. Robinson E, McFarland-Lesser I, Patel Z, Jones A. Downsizing food: a systematic review and meta-analysis examining the effect of reducing served food portion sizes on daily energy intake and body weight. Br J Nutr. 2022 Mar 14;129(5):888. doi:10.1017/S0007114522000903 PubMed PMID: 35387692.

4. Hall KD, Ayuketah A, Brychta R, Cai H, Cassimatis T, Chen KY, et al. Erratum: Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake (Cell Metabolism (2019) 30(1) (67–77.e3), (S1550413119302487), (10.1016/j.cmet.2019.05.008)). Cell Metab. 2019 Jul 2;30(1):226. doi:10.1016/J.CMET.2019.05.020 PubMed PMID: 31105044.

5. Robinson E, Almiron-Roig E, Rutters F, de Graaf C, Forde CG, Smith CT, et al. A systematic review and meta-analysis examining the effect of eating rate on energy intake and hunger. American Journal of Clinical Nutrition. 2014 Jul 1;100(1):123–51. doi:10.3945/ajcn.113.081745 PubMed PMID: 24847856.

6. Lasschuijt MP, Heuven LA, Gonzalez-Estanol K, Siebelink E, Chen Y, Forde CG. The Effect of Energy Density and Eating Rate on Ad Libitum Energy Intake in Healthy Adults—A Randomized Controlled Study. Journal of Nutrition. 2025 Aug 1;155(8):2602–10. doi:10.1016/j.tjnut.2025.06.006 PubMed PMID: 40516651.

7. Andres A, Fisher JO, Anderson CAM, Gardner CD, Giovannucci E, Hoelscher DM, et al. Portion Size and Energy Intake: A Systematic Review [Internet]. 2024 Dec. doi:10.52570/NESR.DGAC2025.SR28 PubMed PMID: 39836778.

8. A A, E G, JO F, C P, HA R, FC S, et al. Frequency of Meals and/or Snacking and Energy Intake: A Systematic Review [Internet] [Internet]. 2024 Dec. doi:10.52570/NESR.DGAC2025.SR10 PubMed PMID: 39812565.

9. Cho S, Kwon H. Current guidelines and future directions in comprehensive obesity assessment. Korean J Fam Med. 2025 Jan 20;47(1):4. doi:10.4082/KJFM.25.0275 PubMed PMID: 41338668.

10. Burr EK, Dvorak RD, de Leon AN, Klaver SJ, Peterson R, Hayden ER, et al. Understanding Loss of Control Eating Through the Lens of Expectancies and Reinforcement Sensitization. Psychiatry. 2024;88(1):55. doi:10.1080/00332747.2024.2403664 PubMed PMID: 39466974.

11. Dicken SJ, Jassil FC, Brown A, Kalis M, Stanley C, Ranson C, et al. Ultraprocessed or minimally processed diets following healthy dietary guidelines on weight and cardiometabolic health: a randomized, crossover trial. Nat Med. 2025 Oct 1;31(10):3297–308. doi:10.1038/S41591-025-03842-0;SUBJMETA PubMed PMID: 40760353.

Dear Reader,

There is a particular kind of frustration that many people know well.

You eat. You try to make reasonable choices. You may even avoid the obvious foods you think you “shouldn’t” eat. And yet, a few hours later, your body is asking for more.

More food. More sweetness. More coffee. More something.

This is often considered as a willpower problem. Usually though, it is a physiological problem. The body keeps asking because the previous meal did not create enough satiety.

In the last articles, we looked at blood sugar, food quality, micronutrients, sleep and stress.

This piece brings those threads together into one functional question: are your daily inputs helping your body feel calm, fuelled, and satisfied, or are they keeping it in a cycle of compensation?

Satiety Is Not Just Fullness

Fullness is the feeling of having food in the stomach.

Satiety is different. It is the signal that the meal was enough: enough energy, enough nutrients, enough satisfaction to stop the search for more.

A large meal can stretch the stomach and create fullness, but if it is low in protein, fibre, or key nutrients, the body may still not register it as satisfying. Fullness tells you there is volume in the stomach. Satiety tells you the body has received enough of what it needs.

A very low-calorie meal can seem like the “right” choice, but leave the body searching for energy, protein, and nourishment. A meal built mostly from carbohydrates can give quick energy - as carbs are broken into sugars and sugar is used for energy - then pivot again into hunger and cravings.

Thalia’s case

Thalia M. was a woman in her mid fifties. She told me she was eating well.

It was the kind of eating most people would call healthy.

Breakfast was usually toast or oats with fruit. Lunch was soup, salad, or something light. Dinner was cooked at home. She was not eating fast food, not drinking fizzy drinks, not buying packets of biscuits for the house.

But by late afternoon, the day’s restraint started to cost her.

She would become restless around food. She would open cupboards without knowing what she wanted. A handful of nuts became several. A square of chocolate became more. If she had wine with dinner, the evening became harder to steer. She described it as “losing discipline”.

When we looked more closely, her meals were not actually holding her.

Breakfast gave quick energy but little protein. Lunch was healthy, but too light. There was fibre, but not enough substance. Fat was either missing completely or arriving later in the evening in a less controlled way. By dinner, she was hungry. She had to catch up.

When we rebuilt the earlier meals of the day: sufficient protein at breakfast, a balanced lunch, enough fluid, and non-alcoholic beer instead of wine, Thalia felt calm around food for the first time in many years.

The Meal Has to Hold

A meal that supports metabolic health usually needs all three macronutrients working in synergy: protein, fat and complex carbs - meaning those with adequate fibre.

Protein helps prolong satiety. It is digested slowly, and sends strong appetite-regulating signals. It is important to add here that as we age, our needs for adequate protein increase rather than decrease.

Fat adds staying power and satisfaction. It slows gastric emptying and makes a meal feel more complete, although it is also energy-dense, so the aim is not “more fat” but the right amount and quality.

Carbohydrate gives quicker energy but is as important as the other macros– especially for satisfaction. The question is what amount suits your current metabolic state? Refined carbohydrate eaten alone gives a fast blood sugar rise and fall; carbohydrate eaten with protein, fat and combined with fibre will satisfy you and sustain energy.

When these parts are poorly balanced, the body may keep looking for what the meal failed to provide.

Below, you will find a practical guide on how to build your metabolism-supporting plate, including the balance of protein, fat, fibre-rich carbohydrates, and ratios.

How to calibrate carbohydrate intake

Is your current carbohydrate intake too much or too little for your current tolerance, activity level and metabolic state?

You may suspect it is too much if meals leave you sleepy, hungry again soon, craving sweet foods, needing caffeine, or feeling mentally foggy. You may also see it in patterns: rising waist circumference, elevated triglycerides, low HDL, higher fasting glucose, rising HbA1c, or large glucose swings if you track them.

The answer is to rebuild the meal: increase your protein, fibre, and fat, decrease carbohydrate quantity and increase their quality by selecting whole unprocessed carbohydrates.

You may suspect carbohydrate is too little if meals leave you physically full but unsatisfied, if your energy drops during the day, or if you feel driven to seek sweetness, bread, snacks or more food later. Some people also notice poorer exercise tolerance, irritability, sleep disruption, constipation, or a sense that meals feel “unfinished.”

Hydration: The Overlooked Signal

Hydration is often treated as a minor detail. It is not.

Mild dehydration can be misread as hunger, fatigue, headache, poor concentration or low energy. It can contribute to constipation, and affect appetite regulation and weight. If you are dehydrated, what feels like a need for food may be partly a need for fluid.

Recent reviews on water intake and weight management suggest that drinking water before meals may reduce perceived hunger, balance appetite and meal energy intake, and trials using about 500 ml before meals have shown greater weight loss in several studies.

A simple test is to notice whether your “hunger” changes after a glass of water and ten minutes. If it disappears, it was probably not true hunger.

Sadly, there is cardiovascular risk from low water intake, most of us know little about.

When you are dehydrated, there is less fluid in your blood. This makes it harder for blood to circulate easily, so the body releases hormones to hold onto water. Those hormones can tighten blood vessels, raise blood pressure, and impair blood sugar regulation. So, habitual low water intake directly contributes to cardio-metabolic strain.

Alcohol Disrupts the System

I mentioned alcohol in Thalia’s case. Alcohol is often separated from food in people’s minds. However, is not separate: It is metabolised as energy, adding about 7 kcal per gram, while it affects appetite, sleep, blood sugar regulation, liver metabolism, and blood pressure.

Alcohol changes decision-making around food. It can make evening eating less controlled, reduce sleep quality, increase next-day cravings and interfere with the liver’s ability to manage glucose and fat metabolism efficiently.

The newer cardiovascular understanding is also very different than the older belief that “moderate drinking may be protective”.

The World Health Organization states that:

There is no safe level of alcohol for health.

Let me repeat that: there is no safe level of alcohol for health.

Recent reviews link alcohol exposure to metabolic dysfunction, inflammation, liver disease, type 2 diabetes risk, contributing to obesity and cardiovascular disease. I have included relevant studies below, for your reference.

For blood pressure specifically, more recent cardiovascular guidance has moved toward reducing or avoiding alcohol as the optimal position for people trying to control this condition.

For those who love to know the mechanisms behind alcohol consumption risk:

Alcohol is metabolised mainly in the liver to acetaldehyde, which promotes oxidative stress and inflammation. This may impair insulin signalling, therefore affect glucose and lipid metabolism, and increase liver fat. In terms of cardiovascular effects, alcohol can raise the sympathetic nervous system activity, and as a result blood pressure, increase arrhythmia risk, and contribute to cardiomyopathy.

Alcohol should not be treated as neutral. In a body already struggling with metabolic or cardiovascular imbalance, alcohol often removes stability from the very systems we are trying to rebuild.

What to Do This Week

I have made it a habit myself and I suggest the same for you. When you put together your plate, observe and calibrate your meals.

At each meal – including snacks – consider:

Read more

Dear reader,

Most of us have heard, in one way or another, that stress affects health deeply. But the word stress is often used too casually. It can mean emotional strain, excessive physical activity, illness, poor sleep, pollution, heat, noise, toxins, infection, or the pressure of living in a state of demand for too long, without recovery and resolution.

The body does not separate these stressors as neatly as we think of them. Emotional stress, physical stress, sickness, and environmental insults all have different entry points, but many of them converge on the same internal systems: the nervous system, the hormonal stress-response system, the immune system, the cells’ energy-producing machinery, blood sugar regulation, blood pressure control, and inflammation.

Don’t think of stress as something only psychological. It is actually biochemical. Over time, repeated activation creates what scientists call allostatic load: the strain that compounds when adaptation is demanded too often, for too long, without sufficient restoration.

Acute stress is not harmful. In the short term, stress hormones help us mobilise energy, sharpen attention, increase cardiovascular output, and prepare the immune system to respond. The problem begins when the body is repeatedly asked to stay in this activated state.

Emotional stress activates the brain’s threat and vigilance systems, which then communicate with the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Cortisol and adrenaline rise. Glucose is released. Blood pressure and heart rate increase. In the short term, this is useful.

When the body stays activated too long

Over time, repeated elevations of cortisol and adrenaline keep the body acting as if it must prepare for demand. Cortisol tells the liver to release more glucose into the blood, while stress hormones make it harder for insulin to move that glucose into muscle and fat cells. This happens partly because the body is prioritising immediate fuel availability over storage and repair. Sleep rhythms become more easily disrupted, appetite and cravings can increase, and blood pressure may rise as the nervous system stays switched on. The immune system can also become less well regulated, allowing low-grade inflammation to persist.

Chronic stress has been linked mechanistically with type 2 diabetes risk, partly through these metabolic and neuroendocrine pathways.

Physical, immune, and environmental stress

Physical stress from activity follows the same principle. Exercise is a stressor, but when dosed well, exercise improves how the body produces energy, handles blood sugar, maintains healthy blood flow, and responds to future stress.

But when training exceeds recovery - especially in the presence of poor sleep, illness, or emotional load - the same adaptive stimulus can become another demand on an already strained physiology.

Sickness creates a different kind of stress. Infection, injury, chronic inflammation, autoimmune activity, and tissue damage all require immune activation. That immune response uses energy. It changes appetite, sleep, glucose handling, temperature regulation, and mitochondrial behaviour.

Environmental stressors add another layer. Air pollution can irritate the lungs and trigger immune signals that spread inflammation through the body. It can also affect the lining of blood vessels, making them less able to relax properly. Some chemicals can interfere with hormone signalling, which may disturb metabolism, appetite, insulin sensitivity, thyroid function, or reproductive hormones.

Recent research suggests that environmental and climate-related stressors can affect the body at a cellular and metabolic level. They may disturb the mitochondria, the parts of the cell responsible for turning food and oxygen into usable energy, and increase oxidative stress: a form of cellular strain that occurs when the body produces more reactive molecules than it can safely neutralise. Over time, these insults can contribute to metabolic syndrome, where blood sugar, blood pressure, abdominal fat, and blood fats begin to shift together, increasing cardiovascular strain.

Chronic stress can drive inflammation

One of the most interesting areas of research is the link between chronic stress and inflammation. Cortisol is usually thought of as a stress hormone, but it also helps calm the immune system once a threat has passed. Under chronic stress, the body may become less responsive to that calming signal. So stress hormones may remain elevated, while the immune system also becomes harder to switch off. The result can be persistent low-grade inflammation: the kind of background immune activity linked with cardiovascular, metabolic, autoimmune, and inflammatory disease.

A useful way to understand the effects of body stressors is that they can all feed into low-grade inflammation. This does not mean obvious inflammation, like the redness and swelling after an injury. It means a subtle, ongoing immune activation in the background. Researchers found that people exposed to more daily stressors had higher levels of inflammation markers such as interleukin-6 and C-reactive protein, both of which are signals that the immune system is more activated, eventually pushing the body toward the same pattern: persistent low-grade inflammation.

What can you do about it?

Stress-management interventions are not just psychological tools. A 2024 meta-analysis found that these interventions can help balance cortisol levels. Meditation research has also shown reductions in markers such as cortisol, C-reactive protein, blood pressure, heart rate, triglycerides, and inflammatory markers.

Breathing is another under-appreciated intervention. Slow breathing and diaphragmatic breathing can improve heart-rate variability, and modestly reduce blood pressure. This way we can directly communicate safety to the nervous system.

Sleep remains foundational, we talked about this in the previous article, because sleep loss itself is a metabolic stressor. It affects glucose regulation, endocrine function, appetite, cortisol rhythm, and recovery. If sleep is chronically disrupted, the body is being asked to repair itself without one of its main repair windows.

Nature exposure is also a crucial element. We don’t need research that shows us how connection to nature, nature-based interventions may reduce stress. Forest-bathing studies have reported lower cortisol, blood pressure, pulse rate, and sympathetic activity in forest environments compared with urban settings.

Intervention decisions

Rather than asking “How do I reduce stress?”, the better question is:

What is my body being repeatedly forced to handle?

If the stress is mental or emotional

If your stress is mental or emotional, begin by reducing what your brain has to keep carrying.

• Write down the three concerns that return most often. Not everything, just those that keep looping. For each one, ask:

• Can this be resolved, supported or accepted somehow?

• If it can be solved, define the next small action. Not the whole solution. Just the next action.

• If you can resolve it with support, name the person, professional, conversation, or resource that could help carry part of it.

• If you can postpone it, decide the date you will return to it. This matters because the brain keeps revisiting unfinished concerns unless it trusts that they have a place to go.

• If you have to accept it, the intervention is not more analysis. It is helping the nervous system stop fighting what cannot be changed today.

Breathing, meditation, prayer, therapy, journaling, time in silence, or a walk without your phone can help. The purpose is to give the body repeated evidence that it is no longer under immediate threat.

A practical starting point is this: take ten minutes each evening to empty your mind onto paper. Then choose one concern only and decide the next action. After that, stop problem-solving. The body needs a boundary between thinking and recovery.

If the stress is environmental

Identify if your environment is causing stress: look at the signals your surroundings are sending your nervous system.

The body is constantly reading the environment: light, noise, clutter, air, temperature, screens, notifications, pace, and interruptions. None of these may feel dramatic on their own, but together they can keep the system in a low-grade state of vigilance.

Start with the parts in the day that can have a bigger impact: your morning and your evening.

In the morning, give your body a clear signal that the day has begun.

• See the daylight as early as possible.

• Open the curtains. Step outside.

• Take a short walk if you can.

This helps anchor circadian rhythm, alertness, mood, and hormonal timing.

In the evening, do the opposite.

• Same time each night, lower the intensity of the environment.

• Dim lights. Reduce screens.

• Silence unnecessary notifications.

• Avoid checking messages that may trigger problem-solving late at night.

• Create a final hour that tells the body: nothing more is required from you today.

• Add one calming repeated action: reading, stretching, breathing, prayer, journaling, or preparing for sleep.

Then look at your physical space. Choose one area that repeatedly creates tension: your desk, bedroom, kitchen counter, inbox, phone, or car, and simplify it. Not the whole house. One area. Environmental stress reduces when the brain no longer has to process constant unfinished signals.

Then track how your body is responding.

Look for signals: easier sleep, less anxiety, feeling calmer, lower resting heart rate, improved blood pressure, better recovery, or simply the feeling that your body is not bracing all the time.

The Aim Is to Reduce the Load

The point is not to “manage stress” in the abstract.

The point is to identify the load, reduce the most unnecessary pressure, and give the body enough consistent signals of safety, so that it does not have to compensate all the time.

This article belongs to Phase 1 of The Metabolic Rebuild, where we are identifying and correcting the most obvious drivers of cardio-metabolic imbalance. In previous articles, we looked at how blood sugar regulation, diet quality, nutrient intake, meal timing and sleep affect metabolic health.

Stress belongs in Phase 1 because the body cannot restore metabolic and cardiovascular balance while it is repeatedly being pushed beyond its capacity to recover.

Feel free to leave a comment on this post and let me know what you’d like to learn more about. I’m all ears and genuinely interested in hearing what you need right now. What you share helps me see what additional support, clarification, and companion pieces may be needed alongside this guidance.

Subscribe now

Bibliography

McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87(3), 873–904. https://doi.org/10.1152/physrev.00041.2006
Supports the explanation of acute versus chronic stress, allostatic load, and the body-wide effects of repeated stress activation.

Joseph, J. J., & Golden, S. H. (2017). Cortisol dysregulation: The bidirectional link between stress, depression, and type 2 diabetes mellitus. Annals of the New York Academy of Sciences, 1391(1), 20–34. https://doi.org/10.1111/nyas.13217
Supports the section linking chronic stress, cortisol dysregulation, insulin resistance, and type 2 diabetes risk.

Yaribeygi, H., Panahi, Y., Sahraei, H., Johnston, T. P., & Sahebkar, A. (2022). Molecular mechanisms linking stress and insulin resistance. EXCLI Journal, 21, 317–334.
Supports the explanation of how stress can impair glucose regulation and insulin sensitivity.

Cohen, S., Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B. (2012). Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proceedings of the National Academy of Sciences, 109(16), 5995–5999. https://doi.org/10.1073/pnas.1118355109
Supports the explanation that chronic stress may reduce the immune system’s responsiveness to cortisol’s anti-inflammatory signal.

Gouin, J. P., Glaser, R., Malarkey, W. B., Beversdorf, D., & Kiecolt-Glaser, J. K. (2012). Chronic stress, daily stressors, and circulating inflammatory markers. Health Psychology, 31(2), 264–268. https://doi.org/10.1037/a0025536
Supports the section on daily stressors and inflammatory markers such as interleukin-6 and C-reactive protein.

Miller, M. R. (2020). Oxidative stress and the cardiovascular effects of air pollution. Free Radical Biology and Medicine, 151, 69–87. https://doi.org/10.1016/j.freeradbiomed.2020.01.004
Supports the discussion of air pollution, oxidative stress, vascular dysfunction, and cardiovascular strain.

Haverinen, E., Fernandez, M. F., Mustieles, V., & Tolonen, H. (2021). Metabolic syndrome and endocrine disrupting chemicals: An overview of exposure and health effects. International Journal of Environmental Research and Public Health, 18(24), 13047.
Supports the section on environmental chemicals, hormone signalling, insulin resistance, and metabolic syndrome.

Heidari, H., et al. (2023). Climate stressors and physiological dysregulations: Mechanistic connections to pathologies. International Journal of Molecular Sciences, 24(24), 17589.
Supports the discussion of climate-related and environmental stressors, mitochondrial dysfunction, oxidative stress, immune disruption, and metabolic syndrome.

Rogerson, O., Wilding, S., Prudenzi, A., & O’Connor, D. B. (2024). Effectiveness of stress management interventions to change cortisol levels: A systematic review and meta-analysis. Psychoneuroendocrinology, 159, 106415. https://doi.org/10.1016/j.psyneuen.2023.106415
Supports the section on stress-management interventions and cortisol regulation.

Garg, P., & Mendiratta, A. (2024). Effect of breathing exercises on blood pressure and heart rate: A systematic review and meta-analysis. International Journal of Cardiology Cardiovascular Risk and Prevention, 20, 200232.
Supports the statement that breathing exercises can modestly reduce blood pressure and heart rate.

Ideno, Y., Hayashi, K., Abe, Y., Ueda, K., Iso, H., Noda, M., Lee, J. S., & Suzuki, S. (2017). Blood pressure-lowering effect of Shinrin-yoku (forest bathing): A systematic review and meta-analysis. BMC Complementary and Alternative Medicine, 17, 409. https://doi.org/10.1186/s12906-017-1912-z
Supports the section on forest bathing, blood pressure, heart rate, and physiological stress reduction.

Dear Reader,

In the last articles, we looked at three core drivers of metabolic and cardiovascular imbalance: blood sugar, diet quality, and dietary micronutrient insufficiencies.

Blood sugar dysregulation, poor diet quality, and micronutrient insufficiencies act together to drive metabolic and overall health imbalances: frequent post-meal glucose spikes and insulin resistance are perpetuated by a diet that is insufficient in fibre, protein, and healthy fats, while common nutrient gaps such as vitamin D, magnesium, B vitamins, and iron may impair energy, metabolism, immune function, and blood sugar control.

Together, they promote weight gain, metabolic syndrome, cardiovascular imbalances, fatigue, and mood disturbances. The practical takeaway is to focus on balancing blood sugar through balanced meals rich in fibre, protein, and minimally processed foods, and to identify and correct nutrient shortfalls through diet.

In this post, I want to introduce the fourth driver: sleep.

Why sleep is a core cardio-metabolic driver

Sleep matters in more than one dimension. Quantity, quality, timing, and regularity each have their own links to blood pressure, glucose regulation, lipids such as cholesterol and triglycerides, body weight, inflammation, and cardiovascular outcomes. Sleep therefore has a central place in cardio-metabolic assessment.

Large observational and meta-analytic studies link poor sleep quantity and quality, as well as irregular sleep, with higher risk of metabolic syndrome, incident diabetes, hypertension, adverse lipid patterns, and cardiovascular events.

Poor sleep blunts the ability of cells to take up and use glucose; that is, it impairs insulin sensitivity. It also increases appetite, may tilt preference towards refined carbohydrates, and so can contribute to blood-sugar imbalances.

Poor sleep does not merely leave one tired; it also alters the body’s internal chemistry. Sleep loss and sleep disruption are linked to higher cortisol, shifts in appetite hormones such as leptin and ghrelin, and a more inflammatory internal state.

Together, these changes can heighten hunger, weaken glucose control, amplify stress signalling, and tilt the body further towards metabolic dysfunction. As a result, it may affect motivation, making good food choices harder to sustain. That means that sleep can either undermine the body’s metabolic resilience and blunt nutritional progress, or strengthen the effects of dietary and micronutrient interventions.

How to recognise whether sleep is a relevant driver for you

A brief self-check is often enough to reveal a sleep issue. Check whether any of the following apply:

• You sleep less than seven hours a night.

• Your sleep is erratic from one night to the next.

• You experience daytime sleepiness.

• You wake up unrefreshed.

• You consistently have trouble falling or staying asleep.

• You snore loudly, gasp, or have pauses in breathing during sleep that are witnessed by others.

The clearer warnings belong with a clinician or sleep clinic: very loud habitual snoring with apnoeas or choking, excessive daytime sleepiness that makes drowsiness unsafe, resistant hypertension, unexplained arrhythmia, or sudden hyper-somnolence.

These raise suspicion of obstructive sleep apnoea or another medical cause.Even with a good diet, targeted micronutrients, and real effort, fasting glucose and blood pressure may remain stubborn. Weight may still rise. Cravings may persist. Daily energy may feel unpredictable, regardless of the diet. When this happens, sleep is often the missing driver.

Intervention decision framework: what to try, and in what order

Begin with the least burdensome steps and give them two to four weeks. For most adults, that means keeping sleep and wake times consistent every day, including weekends, and aiming for seven to nine hours of sleep a night.

Build a simple evening rhythm: dim the lights in your home for the last hour or so before bed, reduce screens and bright light, avoid large late meals and alcohol, and keep caffeine to the earlier part of the day. If you often wake during the night, pay particular attention to the final meal: a very large meal, alcohol, or a meal with insufficient protein may all make sleep less settled.

The bedroom itself should prepare you for a good sleep: cool, dark, quiet, and familiar, with cues that gently tell the body it is time to sleep. If frequent urination is part of the problem, it is also worth reviewing evening fluid intake, the timing of alcohol or caffeine, and any pattern of waking to pass urine that may need medical assessment, especially if it is persistent.

If difficulty falling asleep or staying asleep persists beyond four weeks, or begins to impair your daytime function, you may want to consider cognitive behavioural therapy for insomnia (CBT-I). This is the first-line treatment with the strongest evidence. Where access to CBT-I is limited, a good digital CBT-I programme may be a practical alternative.

If sleep is marked by loud snoring, witnessed pauses in breathing, gasping, excessive daytime sleepiness, or cardio-metabolic problems that remain unusually resistant, obstructive sleep apnoea should be considered. Screening tools such as STOP-Bang can help identify risk (you may want to look this up), but proper assessment requires clinical evaluation and sleep testing, whether at home or in a lab. If sleep apnoea is confirmed, treatment may include CPAP (continuous positive airway pressure machine), weight reduction, positional therapy, or oral appliances.

Short-term aids could have a role, but they should come only after the more fundamental measures described above have been tried. Even then, they are best used as temporary ways to ease the symptom, not resolve the cause. Melatonin or sleep medication may be appropriate in some cases, but they should be used under clinical guidance and medical supervision. They are not root-cause solutions, and they require caution, particularly where other medications or interactions may be involved. Consult your healthcare provider before trying them.

What to expect when you intervene

Sleep rarely transforms everything at once, but it often begins to shift things sooner than people expect. When the improvements are behavioural: a consistent sleep schedule, better evening light habits, a sleep-supportive environment, and, where needed, CBT-I, measurable improvements in sleep quality and sleep efficiency often begin to appear within two to eight weeks. From there, the benefits tend to spread outward: clearer daytime function, better-regulated appetite, and less friction around food choices.

The cardio-metabolic effects of sleep are crucial. Better sleep is associated with improved metabolic health and with improvements in measures such as fasting glucose, insulin sensitivity, and blood pressure. These shifts are meaningful and gather force over weeks and months, especially when sleep is improved alongside diet and micronutrient status rather than in isolation. The response, of course, is individual. But the effect is clear: good sleep acts like an amplifier.

Where obstructive sleep apnoea is present, intervention can change the picture more quickly. CPAP often improves daytime sleepiness early, and may also improve nocturnal blood pressure and some metabolic markers over the following weeks to months. But the benefit depends heavily on adherence. CPAP works best when it is used consistently.

A practical way to begin is simple.

Start with a baseline: keep a sleep diary for seven to fourteen nights and note average sleep time, usual bed and wake times, naps, and caffeine, meal, and alcohol intake. If you already monitor blood pressure or fasting glucose at home, record those too. Then spend the next two to four weeks making improvements to your schedule, strengthening the bedtime routine, and improving the sleep environment.

Follow the decision framework. By weeks three to six, reassess what has changed: energy, cravings, sleep quality, and, if relevant, blood pressure or glucose. If snoring, gasping, or daytime sleepiness persist, pursue evaluation for sleep apnoea. If insomnia remains, move to CBT-I.

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