In January of this year I was feeling awful. No energy, dizzy, nauseous. Just feeling very unwell. Triglycerides 242, ldl 175, hdl 35, h1c 6.0. I was drinking colas daily, eating candy, cookies, cake,.. February I cut out sugar and carbs, started eating lots of protein, started walking daily, resistance bands, chair squats now triglycerides 133, ldl 139, hdl 44, a1c 5.7. I feel so much better.  No dizziness, nausea, so much energy. My nurse practitioner wants me on statins. I refused. I also have lost 25 lbs.  175 to 150.

I reversed my CKD with a carnivore diet (no plant food, no carbs, high fat, moderate protein)
I once asked my first nephrologist, "Is there anything I can do?". He said with a shrug, " just dont each much meat a avoid much salt" I did that and got progressively weaker. My kidneys continued to deteriorate. In my explorations I found many first hand accounts of
people who had used a carnivore diet toreverse the predictable downward spiral towards dialysis, transplant, and often death.

Subsequently, my kidney filtration rate dipped down to 18% (15%=transplant or dialysis. I had told the practice that I would not do dialysis and I was not qualified for transplant. I knew that refusal would result in death in about 10 days, but I was more afraid of disability than death.

On carnivore,my kidney function began to improve. I was out of the danger zone. I became asymptomatic and felt great. I celebrated a new chapter by visiting Thailand, The land of Smiles for 3 months. I joined a wonderful boxing gym and had a ball. I was named, Warrior of the Month. My swan song was a dream come true

Today my kidney filtration rate is 66%, which is normal for my age.

Age 58 1.87 110 Kg (four years ago) stage 2 grade 4 RCC 10.6cm left Kidney, removed. Creatanine rising to 220 over the next two years, life circling the drain, renal appointment to start hemodyalisis.
Didn't make appointment, started Carnivore instead, two months in, pissed out a bottle of "orange fanta", headaches, dizziness disappeared. Age 62, 87kg 8% body fat, excersised until entered beast mode, creatinine in normal range, Hospital baffled, GP baffled, nephrologist baffled, patient happy as a clam

My mom suffered from PKD which ultimately led to renal failure. She was the “ideal” patient - followed all the guidelines including low protein and cranberry juice (lots of it!). She died five years ago after years of dialysis and was still getting the same dietary advice. I wish I had known this information years ago. Thank you for your work and I pray that many people with PKD benefit from it.

It drives me nuts all the misinformation that medical professionals“know“. As a health coach, I am trying to help my clients through activity and nutrition, but because their doctor says what I’m trying to get them to do is ‘wrong’ they won’t listen to me.

Thank you, this was a wonderful podcast. Here in Australia kidney disease has a huge impact on the Indigenous population with dialysis being 11 x higher than for non-Indigenous people. I am Aboriginal and have had many uncles, aunties and cousins go through this and it continues to decimate our people. I was on this path myself and diagnosed with chronic illness. I have been keto for 5 years now and will never go back to processed food. All my illness has gone, I lost 15kg and my immediate family have seen the results and are following keto now. We really need the research to get to the general practitioner doctors in our communities. They take a very authoritarian position and keep perpetuating the myths that there is nothing wrong with high carb/sugar diets.

When I was a medical student in 1987 I was taught that there are often chronic kidney disease changes found in individuals at the time of their diagnosis of type two diabetes. No explanation was offered at the time and I didn't wonder about it I just took it as fact. Many years later when I got interested in Reversing chronic disease I assumed that hyperinsulinemia was what was causing the kidney damage first, then years later added on was damaged from hyperglycemia. The keto diet addresses both.

I found this true. On carnivore, at start eGFR =51, improved to eGFR=64 Do not have polycystic

If it wasn’t for the science presented by the Low Carb Down Under Doctor’s I’d still be living with Type 2 diabetes, be on a host of medications and have a miserable life. I’m now a healthy living example of someone who can prove the science they share works.

Thanks to Dr Mason, I started the carnivore diet. It cured my iron deficiency, brain fog and IBS symptoms reduced to remission. And I lost a lot of weight! I feel so much better! Thank you ❤

I went to the doctor today, 50yo M, said I had started a low carb diet (didnt mention carnivore). He started pushing the Mediterranean diet, lots of leafy stuff, to stay away from animal meat and butter, LOTS of fibre, ect, thats what all the “evidence” shows for healthy heart. I smiled, thanked him. You can’t argue.

Hooray, it’s Christmas before Christmas! A new full length video with so much helpful wisdom from Dr. Paul Mason! Thank you you from the heart for what you’re doing🙏🏽❤️

This is what you will see…..

Senescent cells are damaged cells that stop dividing and accumulate in the kidneys during aging or chronic kidney disease (CKD), driving inflammation and tissue scarring.

How Senescent Cells Affect the KidneyCell Cycle Arrest: Injured renal cells—such as tubular epithelial cells and podocytes—experience persistent DNA damage and permanently stop growing.

SASP Production: These old cells release a harmful mix of inflammatory and profibrotic signals known as the senescence-associated secretory phenotype (SASP).

Fibrosis and Damage: The SASP triggers scarring (fibrosis), blocks normal tissue repair, and forces healthy neighboring cells into secondary senescence.

Emerging TreatmentsSenolytics: Experimental drugs like navitoclax selectively seek out and destroy senescent cells to reduce kidney damage.

Senomorphics: Compounds like metformin suppress the harmful secretions of senescent cells without killing them.

Explore research updates on Kidney Research UK.Review mechanisms of cellular damage in Oxford Academic.Read scientific reviews via PubMed.

Are you looking for information on specific treatments in clinical trials or the biological mechanisms of kidney aging?

https://pubmed.ncbi.nlm.nih.gov/40761301/

Clin Kidney J
. 2025 Jul 7;18(8):sfaf190. doi: 10.1093/ckj/sfaf190. eCollection 2025 Aug.

Understanding and targeting senescence in kidney disease

Lucie Chanvillard 1, Tilly Mason 2, David A Ferenbach 2
Affiliations Expand
PMID: 40761301 PMCID: PMC12319541 DOI: 10.1093/ckj/sfaf190
Abstract
Kidney disease affects >850 million people worldwide and remains a major contributor to patient morbidity, mortality, and healthcare burden. Despite advances in renoprotective therapies, current treatments are largely focused on managing risk factors such as hypertension, hyperfiltration, and hyperglycaemia, with limited options to modify disease progression at the cellular level.

Emerging evidence suggests that cellular senescence, a state of irreversible cell-cycle arrest accompanied by chronic pro-inflammatory signalling, plays a significant role in chronic kidney disease (CKD) pathogenesis, particularly within tubular epithelial cells (TECs). Senescent TECs accumulate in injured kidneys, driving inflammation, fibrosis, and loss of regenerative capacity.

This process is triggered by diverse stressors, including ischaemia-reperfusion injury, metabolic stress, and uremic toxin exposure. The recognition of senescence as a pathological and potentially modifiable process has opened new therapeutic avenues in nephrology.

Preclinical studies demonstrate that senolytics, which selectively eliminate senescent cells, and senomorphics, which suppress the harmful senescence-associated secretory phenotype (SASP), can reduce renal fibrosis and preserve kidney function in experimental models of fibrosis in the kidney and other organs.

Translating these approaches into clinical practice requires overcoming key challenges, including the lack of validated non-invasive biomarkers to monitor renal senescence and the heterogeneity of senescent cells across different disease stages.

This review discusses the contribution of cellular senescence to kidney ageing and disease progression and outlines the underlying molecular mechanisms and biomarkers of renal senescence.

It also highlights recent advances in senotherapeutic strategies, emphasizing future directions for integrating senescence-targeted therapies into comprehensive CKD management.

Keywords: chronic kidney disease; kidney ageing; proximal tubular epithelial cells; renal epithelial senescence; senotherapeutics.

Alpha-lipoic acid (ALA) is a strong antioxidant that may help lower inflammation and protect kidney tissues from oxidative stress, particularly in diabetic kidney disease.

However, medical case reports also link high-dose ALA supplements to rare instances of severe protein-losing kidney damage (membranous nephropathy), meaning it should be used cautiously.

Potential Benefits of Lipoic AcidLess Oxidative Stress: Fights harmful free radicals that hurt kidney cells.

Blood Sugar Support: Helps manage diabetes, which is a major cause of kidney failure.Reduced Inflammation: Lowers specific inflammatory markers linked to chronic kidney disease (CKD) progression.

Risks and ConsiderationsRare Kidney Reactions: Some clinical observations tie ALA use to sudden, biopsy-proven membranous nephropathy and heavy protein in the urine.

Not a Standard Cure: Most protective evidence comes from lab and animal studies; large human trials are still limited.Talk to a Doctor First: Always consult your physician before taking new supplements if you have reduced kidney function.

If you'd like, let me know:

What type of kidney issue or diagnosis you are managingYour current medications or other supplementsI can share more targeted information or help you prepare questions for your doctor.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10097220/

Nutrients. 2023 Apr 1;15(7):1732. doi: 10.3390/nu15071732
Renal-Protective Roles of Lipoic Acid in Kidney Disease
Sulin F Kamt 1, Jiankang Liu 2,3, Liang-Jun Yan 1,*
Editor: Yugo Shibagaki
Author information
Article notes
Copyright and License information
PMCID: PMC10097220 PMID: 37049574
Abstract
The kidney is a crucial organ that eliminates metabolic waste and reabsorbs nutritious elements. It also participates in the regulation of blood pressure, maintenance of electrolyte balance and blood pH homeostasis, as well as erythropoiesis and vitamin D maturation.

Due to such a heavy workload, the kidney is an energy-demanding organ and is constantly exposed to endogenous and exogenous insults, leading to the development of either acute kidney injury (AKI) or chronic kidney disease (CKD).

Nevertheless, there are no therapeutic managements to treat AKI or CKD effectively. Therefore, novel therapeutic approaches for fighting kidney injury are urgently needed.

This review article discusses the role of α-lipoic acid (ALA) in preventing and treating kidney diseases. We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled.

The animal models covered include diabetic nephropathy, sepsis-induced kidney injury, renal ischemic injury, unilateral ureteral obstruction, and kidney injuries induced by folic acid and metals such as cisplatin, cadmium, and iron.

We highlight the common mechanisms of ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death.

It is by these mechanisms that ALA achieves its biological function of alleviating kidney injury and improving kidney function. Nevertheless, we also point out that more comprehensive, preclinical, and clinical studies will be needed to make ALA a better therapeutic agent for targeting kidney disorders.

Keywords: lipoic acid, acute kidney injury, chronic kidney disease, diabetic kidney disease, diabetic nephropathy, nephroprotection

Good video Dr. Shah as you covered all the key risk factors. In terms of risk factors, LDL is by far the lowest risk factor for CVD at 1.38x and diabetes is BY FAR the greatest risk factor at 10.71. If someone has an LDL of 55 or below (which only 3 percent of the population has naturally) and diabetes or metabolic syndrome, they WILL build plaque as they have destroyed their glycocalyx and continually damage the endothelium. The risk factors below point to inflammation being the largest driver of CVD...

Diabetes — 10.71× risk

Metabolic syndrome/Insulin resistance — 6.09× risk

Hypertension — 4.58× risk

Obesity — 4.33× risk

Smoking — 3.92× risk

Family history of MI before 60 — ~1.5–2× risk

Triglycerides — 2.14× risk

ApoB — 1.89× risk

Non-HDL cholesterol — 1.67× risk

LDL cholesterol — 1.38×

>>Two years ago, a 2D echocardiogram revealed coronary calcification, which was preventing one heart valve from closing. My doctor indicated that no surgery was immediately warranted, and the issue would be monitored. I sought some way to address the calcification, and eventually learned about Berberine possibly being able to dissolve the calcification.

I started taking Berberine as a daily supplement about a year ago.

Last month, a follow up ultrasound of my heart found all valves to be functioning normally, and there were no signs of coronary calcification! I am so relieved and glad that it worked. Meanwhile, my cardiologist asked for the second time, “What’s Berberine?”

Go figure.<<

>>My A1C was 6.8 / 8 months ago. I looked for ways other than low carb /exercise which I have been doing already for years to try and help lower my A1C. Came across some good info on Berberine. So I immediately found a respected brand and began taking 500 mg a day. After 8 months and no change in diet/exercise from normal routine my A1C came back at 5.1 on Friday. I was pretty hyped about that. Having any cardiovascular benefits on top would be a bonus.<<

>>I’m 63 male and still work as an industrial mechanic so I’m still very physical every day. I was overweight at 193. In Aug 2022, I had 60% carotid artery blocked on the RH side. My lipids were high but not too crazy, triglycerides 198, total cholesterol 162, non HDL 130. I had been taking many supplements the last few years but stepped up my game with more targeted ones and also stopped eating almost all carbs (SUGAR).

I took 5000MCG Folic Acid, D3/K2, also 10-20IU D3, 2Gram Omega-3, Magnesium, Inositol, Bromelain, Tumeric, then instead of eating Avocado, I ate 2 small servings of fresh Quac, NO CHIPs, every day and ate mainly fish, chicken, meat and eggs. I would eat 3 eggs with a breakfast meat of choice almost every day and would not be hungry until dinner which was just mainly a protein like Salmon or steak.

My doc told me that “those crazy diets will kill you”. Well, when he got the new lipid test results, he had to check to see if they were really mine!!! My tri’s dropped to 79, my total cholesterol to 93 and my non HDL to 52. Then, as a real shocker to even me, my 60% blocked RH carotid was almost clear of all blockage, so minimal that it was well below 5% or so my doc said.

He just told me to keep doing what I am doing and really did not care to ask mw how I did this since he told me that I would kill myself by my eating almost no carbs. He knew all my other supplements and had no issue with them. I really do not know what was the main reason for my way, way better results. I lost 23 pounds and feel great, I have the best lipid panel since it was tested in my 40’s.<<

>>I am no doctor and cannot say what will work best for other people but I do know that limiting the carbs to almost nothing is probably the best thing a person can do. Most people forget about all the hidden in plain sight carbs, like the so called “energy drink”. Many have close to 400 calories of sugar and caffeine. You want a little extra kick in the middle of the day, why not just have a cup of coffee of tea, no sugar or milk?????<<

>>This was not easy being 63 and eating bread, rice , pasta all my life, but as my body changed, so did my cravings. Try it, what do you have to lose but a few pounds?????? While I am aware of the benefits of berberine, I have to be careful in taking it due to familial high BP which I take meds for. I also was able to take less of my BP meds after my weight loss and am working on taking less still.<<

>>My dad took both Metformin and Berberine. Metformin affected his kidneys negatively and his blood markers for cholesterol and liver were not great . With Berberine his cholesterol levels went down and his liver markers improved and his kidneys too<<

>>For type 2 diabetics , the use of berberine along with K2 +D3 supplements, healthy eating and exercise is very helpful at removing arterial plaque . Just make sure you don’t go overboard on dosage and eat consistently healthy.<<

>>I started taking 500mg twice a day of berberine (along with diet and exercise) about a year ago for mildly elevated A1C. My A1C has completely normalized, but more surprisingly there was a huge impact on my mental health. Since childhood I’ve struggled with depression and a very poor memory.

My wife has always joked about how bad my memory is even though I’m in my 30s. My memory is better than hers now, and my depression has been in remission for a year. And every time I back off on the berberine my memory and mood get worse over a few weeks.<<

My mother experienced cognitive decline caused by atorvastatin, and the doctor seized the opportunity to destroy her further by prescribing donepezil hydrochloride. After losing her mind, my mother passed away a year later.…

My mom developed Diabetes a month after taking statins. She also developed dementia.

Try measuring heart attacks as a function of sugar and insulin concentration instead and I'm sure you'll get a nice straight line.

Even success would have been failure. IL-6 is a myokine as well, so inhibiting it means, to mention an extreme, muscle wasting. Exercise won't prompt the proper responses. A longer-term study would likely have been a disaster. The heart is also a muscle.

I had a MI event in 2000, LAD 2 stents. Felt the onset again in 2024, 3 stents. High enough doses of statins that I had to take them at night as they affected my brain so severely in the first 4 hours or so after taking them that I couldn't work effectively. Did they help? Well in 2016 I had a quintuple bypass, so I guess the answer is no. Been working the anti-inflammatory route and my stress test 6 months ago was an all clear. To keep my cardiologist happy, I am on 20 mg of Rosuvastatin because, as I understand it, it does not cross the blood/brain barrier. And I'm on COQ10 to counter some of it's effects on the liver.

Don't even get your lipids tested. Have you seen the recent video on Dave Mac's channel with Drs Sam and Mark Bailey? I suggested he did an interview with them. I have now suggested he does one with Dr Andrew Kaufman.

>>To say LDL, in particular apo(b) plays no role whatsoever in heart disease is the classic grift. You get people letting their LDL get sky high and think they are OK for some magic metabolically healthy lie spread by places like this. Usually non MD's.

Small dense LDL (sdLDL) is what needs to be reduced as much as possible.
What IS neccessary for health are the large buoyant (lbLDL) - thus suppressing these via statins makes no sense.

Statins do have a small anti-inflammatory effect - some people use a small dose 5mg every other day (but there are better options re anti-inflammatory role: consider colchicine 0.3-0.5mg per day).
Ref Dr Rob Cywes MD PhD.

Overall, statins are totally not worth it for many people because of the big negative side-effects: pain/cramps, muscle weakness (heart is also a muscle), cognitive degradation, push towards insulin resistance / diabetes T2…

The above LDL particle differentiation can be done for the past more than 20 years via NMR LDL particle test.

For example, just knowing the NMR sdLDL 1800 nmol/L (number of particles per volume) tells a huge story - getting into high cvd risk factor (anything above 200 nmol/L begins to be concerning).

Also:
Need triglycerides less than 60mg/dL - stop eating grains (esp modern wheat), sugars and restrict carbs (not refined) to 15g / day.

Eat REAL food: beef, small fish, eggs, hard cheeses, anions, chia seeds (for fiber), supplement zinc, magnesium, vit C build up to 5g+ per day, vit B complex, vit A, D3, E, K2.

Eat fish oil EPA/DHA - 4g+ per day.
[ A triglycerides reading of 60 mg/dL converts to 3.3 mmol/L in UK units (millimoles per litre).
You get this number by dividing the mg/dL value by 18 ].
Ref: Dr William Davis MD<<