Anyone on Keto?

[Judy Reneau]

My blood sugar started going up. I'm 82 and it finally caught up with me so I ha no choice but to go Keto. Now my fasting reading is in the 70's.

[Todd Allen]

59 and I have been keto for 8 years and wish I had tried it much sooner.  It's not a popular dietary regimen here especially the animal protein centric variety that I now follow.  Most here are vegetarian or vegan.  I did that for too many years and while much of the damage I suffered might have been avoidable with better choices I doubt I could have ever achieved the results I am getting now.  My suggestion to all is chase whatever improves how you feel, perform and look in the mirror.  It's not the same for everyone and it may change throughout ones stages of life.

[Dean Pomerleau]

Fair enough Todd. That seems like pretty reasonable advice and I'm glad meat-heavy keto has worked so well for you. But you should make it clear when you make a post like this that your health situation is pretty unusual. 

[Todd Allen]

On 1/30/2024 at 5:14 AM, Dean Pomerleau said:

But you should make it clear when you make a post like this that your health situation is pretty unusual. 

I have SBMA aka Kennedy's disease a neuromuscular wasting disease attributed to an expanded CAG repeat in the androgen receptor gene with a recognized rate of occurrence of about 1 in 40,000.  But much of the phenotype is essentially metabolic syndrome which is common in advanced age especially among populations eating diets rich in highly processed foods such as grain derived refined sugars, starches and oils.  There is a CDC estimate that more than 80% of American seniors are affected by metabolic syndrome.  In SBMA I believe mitochondrial dysfunction in muscle starts early aggravating blood sugar regulation resulting in hyperinsulinemia and unhealthy fat accumulation first in muscle but then leading to hypertrophic subcutaneous adipose, fatty liver and other visceral fat accumulations which appear to cause cascading harms in every tissue where excess lipids concentrate.  In people without SBMA this sequence might start with hypertrophic subcutaneous adipose or fatty liver with intramuscular fat infiltration and sarcopenia being later stages of the progression.

Despite the widely held belief that dietary fat and especially animal sourced and saturated fats are the worst culprits for excess especially ectopic fat accumulation and all related harms a large and growing number of people including myself find it possible to reverse these problems when aggressively restricting carbohydrates which can only be done eating a fat based diet.  I have transitioned to mostly animal fats because I see a modest improvement in muscle with higher levels of animal proteins and low muscle mass is my primary health concern.  Poor muscle health is common in very advanced age but it is usually accompanied by other health concerns which might suggest different dietary priorities.

[Dean Pomerleau]

Thanks Todd. That was well explained, including the perspective that others without Kennedy's disease might nevertheless get into a similar metabolic state and benefit from a keto diet.

I don't think there is any doubt that the human body is a flex fuel vehicle that can operate on many different inputs, and there is no doubt that cutting out carbs will reduce blood sugar dramatically in people with impaired glucose metabolism.

Putting aside concerns about animal welfare and the environmental impact of animal agriculture, my biggest reservations about a high-fat, animal-based keto diet is whether or not it contains adequate micro-nutrients for long-term health, many of which are found (mostly) in plant foods that are often left out of a keto diet like yours. But obviously a similar criticism can be leveled at a poorly planned vegan diet (e.g. lack of B12).

 

[Todd Allen]

18 hours ago, Dean Pomerleau said:

Putting aside concerns about animal welfare and the environmental impact of animal agriculture, my biggest reservations about a high-fat, animal-based keto diet is whether or not it contains adequate micro-nutrients for long-term health, many of which are found (mostly) in plant foods that are often left out of a keto diet like yours.

My wife and I share concerns for animal welfare, environmental impact and adequate micro nutrient content of diet.  Our concerns about animal welfare stem mainly from animal husbandry practices of conventional agriculture and we address that by minimizing our purchase of those products.  When we avoid going to grocery stores and restaurants we also minimize the amount of food we consume that has been shipped extreme distances and produced via exploitation of other people and lands.

As for micro-nutrients I suspect the products of animals raised on forage is somewhat better to those raised in feedlots.  We somewhat offset higher cost by eating a lot of offal which has a big impact on nutritional profile.  Look up various forms of liver, kidney, heart, etc. in cronometer and you will find these are nutritionally dense foods.  Cronometer does not address bioavailibilty of micro-nutrients but those from animal sources tend to be more readily absorbed.  We minimize waste by not trimming fat, skin or gristle, consuming drippings rendered in cooking and further rendering bones and other scraps which gleans additional nutrients while reducing cost and impact.  We consume a significant quantity of greens, herbs, spices and lower carb vegetables and even some fruit especially fruits commonly referred to as vegetables.  While they contribute modestly to our caloric needs they have considerable micro-nutrients and their profiles tend to cover weaknesses in our animal foods such as folate.  The only shortfalls I commonly see in cronometer are vitamins C, D & E.  I supplement C with bulk ascorbic acid and ascorbyl palmitate powders.  I supplement D when I get inadequate sun.  I used to supplement E but through testing have come to believe it is not needed and stopped although I don't know if it is because some of my foods are unknowingly high in E or my combination of very high levels of lipoproteins, albumin and high vitamin C intake keeps my vitamin E elevated.

[Judy Reneau]

I weigh 110 pounds and my BMR is 960 calories. On Keto that makes 200 calories of protein a day. The eggs, cheese, and meat are all grass-fed.

[mccoy]

On 1/26/2024 at 8:31 PM, Judy Reneau said:

My blood sugar started going up. I'm 82 and it finally caught up with me so I ha no choice but to go Keto. Now my fasting reading is in the 70's.

Ketogenic diets, if practiced for long periods, may be a way to swap one problem with another equally, or more serious. You may be swapping prediabetes with hypercholesterolemia. Not to speak about a weakening of immunity functions, due to the lack of phytonutrients. Not to speak about other issues mentioned by Dom D'Agostino, one of the top serious authorities on keto, in the lengthy interview with Rhonda Patrick (one of such issues is death).

I don't have an answer for your increasing blood sugar. I tried moderate carbs and it worked, but I have the considerate suspicion that other bodily functions are not working on an optimal level, and am switching back to a diet with some fresh fruit and a little cereals, less protein. Still work in progress. I do not share, for various reasons, the views of the vegan doctors who advocate a very low fat diet, although that might be efficacious in some cases. Most of it is anecdotal though and extremes usually do not work well with everyone.

Losing weight is not always a solution, since you clearly have no superfluous weight to loose, neither do I. I have yet to evaluate my present FG, I keep forgetting about measuring it regularly.

I am going to try reasonable lifestyle adjustments (I'm not retired and I cannot walk all day long, nor I can have very regular sleep) but if my FG goes on increasing, my solution will be to consult a diabetologist, eventually taking some drugs like canaglifozlin, but not metformin.

Edited February 4 by mccoy

[Ron Put]

On 2/2/2024 at 6:12 AM, Judy Reneau said:

I weigh 110 pounds and my BMR is 960 calories. On Keto that makes 200 calories of protein a day. The eggs, cheese, and meat are all grass-fed.

There is a reason why most here are vegetarian or vegan -- it has to do with overwhelming evidence in favor of such diets for health and longevity.

Here is a summary of ketogenic diets that includes a paragraph on long-term insulin resistance:

 

Ketogenic Diets and Chronic Disease: Weighing the Benefits Against the Risks

Type 1 Diabetes

Although ketogenic diets can improve glycemia in pediatric patients with type 1 diabetes, they are generally not used in this population due to the risk of malnutrition, failure to thrive, reduced bone density, hyperlipidemia, poor sleep, amenorrhea, and hypoglycemia. In addition, mood and behavior may be adversely affected (33).

In adults with type 1 diabetes, both favorable and unfavorable outcomes have been observed. A small study of 11 adults with type 1 diabetes reported that a ketogenic diet improved blood glucose control (34). However, the ketogenic diet triggered more frequent and extreme hypoglycemic episodes (6.3 episodes per week compared to 1–2 episodes per week typically reported for those following conventional or otherwise unspecified diets). The majority of participants also developed dyslipidemia. Lipid changes are of particular concern in individuals with diabetes, who are already at heightened risk of cardiovascular events (34).

A comprehensive review strongly discouraged sustained ketosis or hyperketonemia in individuals with type 1 diabetes (35). Due to metabolic irregularities associated with type 1 diabetes, ketone production is elevated, and ketone clearance is diminished. Individuals with elevated ketones are at increased risk for complications of the microvasculature, brain, kidney, and liver compared to those with normal ketone levels. In type 1 diabetes, hyperketonemia is associated with oxidative stress, inflammation, non-alcoholic fatty liver disease, and insulin resistance (35).

Type 2 Diabetes

Management

Ketogenic diets depress appetite, promote weight loss, reduce blood glucose values, and decrease HbA1c in the short term (21, 36–43). Some studies have reported improved insulin sensitivity (40); the effect appears to be dependent on loss of fat mass (44). In the abovementioned metabolic ward study in which 17 overweight or obese men were provided a baseline diet (50% carbohydrate) for 4 weeks and then a ketogenic diet (5% carbohydrate) for 4 weeks, during the ketogenic diet phase, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and C-reactive protein increased significantly, while fasting insulin and triglycerides decreased. While on the ketogenic diet, insulin sensitivity was impaired when participants were challenged with a baseline diet meal (50% carbohydrates) (45).

In the 2021 metabolic ward trial by Hall et al. comparing the effects of an animal-based ketogenic diet and a plant-based, low-fat diet, the plant-based diet had a greater glycemic load and predictably resulted in higher postprandial glucose and insulin levels than the ketogenic diet. However, glucose tolerance, as determined by an oral glucose tolerance test at the end of each phase, was compromised during the ketogenic phase (average 2-h glucose was 142.6 mg/dL) compared to the plant-based phase (average 2-h blood glucose was 108.5 mg/dL). In addition, high-sensitivity C-reactive protein, a marker of inflammation, was substantially higher while on the ketogenic diet compared to the plant-based diet (2.1 vs. 1.2 mg/L; p = 0.003), although not significantly different from baseline (27).

Another low-carbohydrate diet trial that followed individuals for 1 year found that insulin sensitivity was improved at 6 months but returned to baseline at 1 year (22). In healthy men, a ketogenic diet (83% fat and 2% carbohydrate) reduced insulin's ability to suppress endogenous glucose production (46).

A recent meta-analysis showed that reductions in hemoglobin A1c achieved with carbohydrate-restricted diets typically wane after a few months and that such diets are not more effective than other diets (47).

In other clinical trials with ketogenic diets, diabetes medications are frequently reduced or eliminated (21, 36–43). The beneficial effects of ketogenic diets for people with type 2 diabetes are attributable primarily to weight loss, with benefits appearing to wane over time (48, 49). Few additional negative impacts on global measures of health have been reported in short-term studies on type 2 diabetes (21, 37, 40). Long-term effects have not been elucidated (49).

[Todd Allen]

On 2/2/2024 at 8:12 AM, Judy Reneau said:

BMR is 960 calories. On Keto that makes 200 calories of protein a day.

Your BMR and protein intake strike me as low although both might be reasonable and perhaps even conducive to longevity for a smaller, elderly woman.  I would point out though that the commonly given advice towards limiting protein to about 20% of calories on a ketogenic diet is based on helping a very wide range of people including those who are in poor metabolic health achieve ketosis.  I am currently doing well with protein at about 25% of caloric intake on about 1900 calories/day at a body weight of 125 lbs.  I know many do well at significantly higher intakes of both calories and protein with respect to body weight.

[Todd Allen]

14 minutes ago, Ron Put said:

Here is a summary of ketogenic diets that includes a paragraph on long-term insulin resistance:

This is a summary by Neal Barnard, a vegan advocate, who likely lacks significant personal experience with ketogenic diets and someone who has little credibility among the cohort of physicians who follow ketogenic diets and those prescribing ketogenic diets for their patients.

[Ron Put]

9 hours ago, Todd Allen said:

This is a summary by Neal Barnard, a vegan advocate, who likely lacks significant personal experience with ketogenic diets and someone who has little credibility among the cohort of physicians who follow ketogenic diets and those prescribing ketogenic diets for their patients.

Todd, what I posted is fairly well-accepted and it makes sense for the majority of people who want to stay healthy..

The excerpt is also pretty well-supported, feel free to review the citations. Attacking the author because he is vegan and "has little credibility among the cohort of physicians who follow ketogenic diets" is not addressing the core argument, but it's an ad hominem jab... 😞

I posted some more studies on insulin resistance and high-fat diets in the Oreos thread.

 

[IgorF]

Thinking about insulin resistance as thought to be the first thing in the t2d path I wondered - how this could be applied to the case described by the topic starter (no overweight, sound dieting, etc.). It seems there is a plausible explanation nicely visualized in Gerald Shulman's article "Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease" (https://doi.org/10.1056/nejmra1011035 could be fetched via scihub)

Actually aging mitochondria could be the source of the process illustrated with:

And this raises another question - what effect will switching to keto produce in advanced age? I think mitochondria degradation is a consensus as a "hard rate limiter" for all forms of life that raised from this model and there is no way to avoid going into "prediabetes" with aging, but if it is about blood markers and clinical picture is not supported with all known risk factors I would personally go with higher morning glucose levels than trying to go keto. That is not an advice offcourse, that is how I think I will do in the future (if I will face the need to do this choice).

 

Br,

Igor

 

 

[Todd Allen]

20 hours ago, Ron Put said:

what I posted is fairly well-accepted

No it isn't.  It is considered an example of the idiocy or evil dishonesty of a vegan.

 

20 hours ago, Ron Put said:

I posted some more studies on insulin resistance and high-fat diets

HFDs are not keto and all of the ingredients are things people considering keto are warned not to eat.  The HFD is a research diet designed to produce disease in mice and it is much closer to your diet than mine.

Edited February 5 by Todd Allen

[Gordo]

Are there any "Longevity Olympians" or SuperCentenarians that would be considered long term "Keto" people?

Honest question.  I have not heard of a single one, but I didn't exactly do any sort of deep research.

[Gordo]

I would think a high protein keto diet would result in high IGF-1

Optimal IGF-1 Levels for Longevity (link)

The relationship between IGF-1 levels and health is somewhat complicated. Excessively low or high IGF-1 levels could lead to health problems. In adults, a high IGF-1 level is linked to accelerated aging and an increased risk of cancer and premature death.^1-5 Maintaining a relatively low IGF-1 level throughout most of one’s adult life is thought to be an important factor by which centenarians are able to live that long without developing cancer.

However, low IGF-1 in the elderly is linked to frailty and disease risk as well. Adequate IGF-1 levels are required for maintenance of bone mass, muscle mass and brain function at later ages. ^6-8

So to prolong our lifespan, the goal is to maintain a relatively low IGF-1 throughout most of our adult life, and then as we get into our eighties and beyond, to consume enough protein so that our IGF-1 level does not get excessively low.

It is important to pay attention to our diet, to ensure our IGF-1 levels are favorable throughout life.

How IGF-1 works in our body

IGF-1 stands for insulin-like growth factor 1. It is a hormone with a similar structure to insulin. IGF-1 is a cell growth-promoter, important during childhood, contributing to brain development and muscle and bone growth. Growth hormone (GH) from the pituitary gland stimulates IGF-1 production in the liver; IGF-1 levels peak during our teen years and twenties, and then levels decline with age.

Circulating IGF-1 is also regulated by dietary protein intake, especially animal protein. Animal protein is more biologically complete, meaning it has high levels of all essential amino acids, so it can trigger excessive body production of IGF-1, whereas plant protein does not.^9-10 High-glycemic, refined carbohydrates can also raise IGF-1.^11-13

Optimal IGF-1 levels

A meta-analysis analyzed ten studies on IGF-1 levels and all-cause mortality. The authors found a “U-shaped” association, meaning that IGF-1 levels on the low end and the high end of the spectrum were associated with increased risk of premature death.¹⁴

The lowest risk was at the 55th percentile of serum IGF-1, and increased in both directions for all-cause, cancer, and cardiovascular mortality.¹⁴ This data suggests that we should aim for an IGF-1 level near the lower to middle for healthy people in our age range. A few studies, primarily in European populations, have attempted to define average IGF-1 levels for healthy people in different age ranges:^15-17

Age:	Average Serum IGF-1 (ng/ml)
21-30	158-230
31-40	135-220
41-50	121-193
51-60	98-150
61-70	85-140
71-80	85-95
80+	85-90

These numbers are somewhat lower than the average IGF-1 levels reported in several other studies in U.S. and European populations.

The European Prospective Investigation into Cancer and Nutrition (EPIC) study reported an average serum IGF-1 level of 200-210 ng/ml, suggesting that this is a typical level for adults on a Western diet.¹⁸ The amount of animal products consumed by most Americans drives their IGF-1 into this danger zone (above 200), increasing their risk of cancer.

Two studies comparing adults on a vegan (or raw vegan) diet (9-10 percent of calories from protein, no animal protein) to those on a Western diet (16-17 percent of calories from protein) found the Western diet average IGF-1 level of 200 ng/ml and vegan average lower than 150 ng/ml. One of these studies also evaluated IGF-1 in non-vegan endurance runners, and their average was about 175.^19-20 The average age of subjects in these studies was in the mid-50s.

Low IGF-1 levels associated with an increased risk of disease or mortality are generally about 70-80 ng/ml or lower.^15,21-26 Studies in elderly men (average age 75) have found increased risk of cardiovascular events and deaths from cancer in high IGF-1 groups, approximately 190 ng/ml.^22-23

In the Nurses’ Health Study, premenopausal women with IGF-1 levels higher than 207 had a substantially higher risk of breast cancer.^2,7 In the Physicians’ Health Study, there was an increase in prostate cancer risk once IGF-1 increased above 185 ng/ml.²⁸

Taking all of this information into account, for most adults, keeping IGF-1 below 175 ng/ml is likely important, and below 150 ng/ml should be even more protective. Serum IGF-1 levels below 80 ng/ml may be detrimental, especially after the age of 75.

Restricting animal protein during most of one’s adult life to maintain a relatively low, but not excessively low IGF-1, is an important objective for those desiring superior health and life extension.  Protein assimilation can decline in the elderly. The use of greens, seeds and beans in the Nutritarian diet, to assure protein adequacy with aging, prevents the excessive lowering of IGF-1 in the elderly, often seen with other plant-based diets. The attention to micronutrient completeness and plant protein adequacy on a Nutritarian diet makes it the most scientifically supported diet-style to push the envelope of human longevity.

 

References

1. Chitnis MM, Yuen JS, Protheroe AS, et al. The type 1 insulin-like growth factor receptor pathway. Clin Cancer Res 2008,14:6364-6370. 
2. Werner H, Bruchim I. The insulin-like growth factor-I receptor as an oncogene. Arch Physiol Biochem 2009, 115:58-71.
3. Davies M, Gupta S, Goldspink G, Winslet M. The insulin-like growth factor system and colorectal cancer: clinical and experimental evidence. Int J Colorectal Dis 2006, 21:201-208. 
4. Sandhu MS, Dunger DB, Giovannucci EL. Insulin, insulin-like growth factor-I (IGF-I), IGF binding proteins, their biologic interactions, and colorectal cancer. J Natl Cancer Inst 2002, 94:972-980. 
5. Kaaks R. Nutrition, insulin, IGF-1 metabolism and cancer risk: a summary of epidemiological evidence. Novartis Found Symp 2004, 262:247-260; discussion 260-268.  
6. Lamberts SW, van den Beld AW, van der Lely AJ. The endocrinology of aging. Science 1997, 278:419-424. 
7. Doi T, Shimada H, Makizako H, et al. Association of insulin-like growth factor-1 with mild cognitive impairment and slow gait speed. Neurobiol Aging 2015, 36:942-947. 
8. Calvo D, Gunstad J, Miller LA, et al. Higher serum insulin-like growth factor-1 is associated with better cognitive performance in persons with mild cognitive impairment. Psychogeriatrics 2013, 13:170-174. 
9. Thissen JP, Ketelslegers JM, Underwood LE. Nutritional regulation of the insulin-like growth factors. Endocr Rev 1994,15:80-101. 
10. Clemmons DR, Seek MM, Underwood LE. Supplemental essential amino acids augment the somatomedin-C/insulin-like growth factor I response to refeeding after fasting. Metabolism 1985, 34:391-395. 
11. Runchey SS, Pollak MN, Valsta LM, et al. Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study. Eur J Clin Nutr 2012, 66:1146-1152. 
12. Brand-Miller JC, Liu V, Petocz P, Baxter RC. The glycemic index of foods influences postprandial insulin-like growth factor-binding protein responses in lean young subjects. Am J Clin Nutr 2005, 82:350-354. 
13. Biddinger SB, Ludwig DS. The insulin-like growth factor axis: a potential link between glycemic index and cancer. Am J Clin Nutr 2005, 82:277-278. 
14. Burgers AM, Biermasz NR, Schoones JW, et al. Meta-analysis and dose-response metaregression: circulating insulin-like growth factor I (IGF-I) and mortality. J Clin Endocrinol Metab 2011, 96:2912-2920. 
15. Ranke MB, Osterziel KJ, Schweizer R, et al. Reference levels of insulin-like growth factor I in the serum of healthy adults: comparison of four immunoassays. Clin Chem Lab Med 2003, 41:1329-1334. 
16. Bidlingmaier M, Friedrich N, Emeny RT, et al. Reference intervals for insulin-like growth factor-1 (igf-i) from birth to senescence: results from a multicenter study using a new automated chemiluminescence IGF-I immunoassay conforming to recent international recommendations. J Clin Endocrinol Metab 2014, 99:1712-1721. 
17. Brabant G, von zur Muhlen A, Wuster C, et al. Serum insulin-like growth factor I reference values for an automated chemiluminescence immunoassay system: results from a multicenter study. Horm Res 2003, 60:53-60. 
18. Crowe FL, Key TJ, Allen NE, et al. The association between diet and serum concentrations of IGF-I, IGFBP-1, IGFBP-2, and IGFBP-3 in the European Prospective Investigation into Cancer and Nutrition. Cancer Epidemiol Biomarkers Prev 2009,18:1333-1340. 
19. Fontana L, Klein S, Holloszy JO. Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk. Am J Clin Nutr 2006, 84:1456-1462. 
20. Fontana L, Weiss EP, Villareal DT, et al. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Aging Cell 2008, 7:681-687. 
21. Friedrich N, Haring R, Nauck M, et al. Mortality and serum insulin-like growth factor (IGF)-I and IGF binding protein 3 concentrations. J Clin Endocrinol Metab 2009, 94:1732-1739. 
22. Carlzon D, Svensson J, Petzold M, et al. Both low and high serum IGF-1 levels associate with increased risk of cardiovascular events in elderly men. J Clin Endocrinol Metab 2014, 99:E2308-2316. 
23. Svensson J, Carlzon D, Petzold M, et al. Both low and high serum IGF-I levels associate with cancer mortality in older men. J Clin Endocrinol Metab 2012, 97:4623-4630. . 
24. van Bunderen CC, van Nieuwpoort IC, van Schoor NM, et al. The Association of Serum Insulin-Like Growth Factor-I with Mortality, Cardiovascular Disease, and Cancer in the Elderly: A Population-Based Study. J Clin Endocrinol Metab 2010. 
25. Arai Y, Takayama M, Gondo Y, et al. Adipose endocrine function, insulin-like growth factor-1 axis, and exceptional survival beyond 100 years of age. J Gerontol A Biol Sci Med Sci 2008, 63:1209-1218. 
26. Johnsen SP, Hundborg HH, Sorensen HT, et al. Insulin-like growth factor (IGF) I, -II, and IGF binding protein-3 and risk of ischemic stroke. J Clin Endocrinol Metab 2005, 90:5937-5941. 
27. Hankinson SE, Willett WC, Colditz GA, et al. Circulating concentrations of insulin-like growth factor-I and risk of breast cancer. Lancet 1998, 351:1393-1396. 
28. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 1998, 279:563-566.

[Gordo]

Keto influencers seem to die on the younger end of the spectrum of all diet influencers:

 

 

[drewab]

7 hours ago, Gordo said:

Keto influencers seem to die on the younger end of the spectrum of all diet influencers:

 

 

This is an incredibly informative video (along with part 1 and 3). It's well worth the hour of watching. The amount of time, effort, and researchers that went into this is remarkable!

[Ron Put]

12 hours ago, drewab said:

This is an incredibly informative video (along with part 1 and 3). It's well worth the hour of watching. The amount of time, effort, and researchers that went into this is remarkable!

It supports all the population studies that generally indicate that longevity is highest in communities with high whole carbohydrates, and correspondingly low animal protein and fat consumption.

[Saul]

On 2/4/2024 at 4:08 PM, Ron Put said:

There is a reason why most here are vegetarian or vegan -- it has to do with overwhelming evidence in favor of such diets for health and longevity.

Here is a summary of ketogenic diets that includes a paragraph on long-term insulin resistance:

 

Ketogenic Diets and Chronic Disease: Weighing the Benefits Against the Risks

Type 1 Diabetes

Although ketogenic diets can improve glycemia in pediatric patients with type 1 diabetes, they are generally not used in this population due to the risk of malnutrition, failure to thrive, reduced bone density, hyperlipidemia, poor sleep, amenorrhea, and hypoglycemia. In addition, mood and behavior may be adversely affected (33).

In adults with type 1 diabetes, both favorable and unfavorable outcomes have been observed. A small study of 11 adults with type 1 diabetes reported that a ketogenic diet improved blood glucose control (34). However, the ketogenic diet triggered more frequent and extreme hypoglycemic episodes (6.3 episodes per week compared to 1–2 episodes per week typically reported for those following conventional or otherwise unspecified diets). The majority of participants also developed dyslipidemia. Lipid changes are of particular concern in individuals with diabetes, who are already at heightened risk of cardiovascular events (34).

A comprehensive review strongly discouraged sustained ketosis or hyperketonemia in individuals with type 1 diabetes (35). Due to metabolic irregularities associated with type 1 diabetes, ketone production is elevated, and ketone clearance is diminished. Individuals with elevated ketones are at increased risk for complications of the microvasculature, brain, kidney, and liver compared to those with normal ketone levels. In type 1 diabetes, hyperketonemia is associated with oxidative stress, inflammation, non-alcoholic fatty liver disease, and insulin resistance (35).

Type 2 Diabetes

Management

Ketogenic diets depress appetite, promote weight loss, reduce blood glucose values, and decrease HbA1c in the short term (21, 36–43). Some studies have reported improved insulin sensitivity (40); the effect appears to be dependent on loss of fat mass (44). In the abovementioned metabolic ward study in which 17 overweight or obese men were provided a baseline diet (50% carbohydrate) for 4 weeks and then a ketogenic diet (5% carbohydrate) for 4 weeks, during the ketogenic diet phase, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and C-reactive protein increased significantly, while fasting insulin and triglycerides decreased. While on the ketogenic diet, insulin sensitivity was impaired when participants were challenged with a baseline diet meal (50% carbohydrates) (45).

In the 2021 metabolic ward trial by Hall et al. comparing the effects of an animal-based ketogenic diet and a plant-based, low-fat diet, the plant-based diet had a greater glycemic load and predictably resulted in higher postprandial glucose and insulin levels than the ketogenic diet. However, glucose tolerance, as determined by an oral glucose tolerance test at the end of each phase, was compromised during the ketogenic phase (average 2-h glucose was 142.6 mg/dL) compared to the plant-based phase (average 2-h blood glucose was 108.5 mg/dL). In addition, high-sensitivity C-reactive protein, a marker of inflammation, was substantially higher while on the ketogenic diet compared to the plant-based diet (2.1 vs. 1.2 mg/L; p = 0.003), although not significantly different from baseline (27).

Another low-carbohydrate diet trial that followed individuals for 1 year found that insulin sensitivity was improved at 6 months but returned to baseline at 1 year (22). In healthy men, a ketogenic diet (83% fat and 2% carbohydrate) reduced insulin's ability to suppress endogenous glucose production (46).

A recent meta-analysis showed that reductions in hemoglobin A1c achieved with carbohydrate-restricted diets typically wane after a few months and that such diets are not more effective than other diets (47).

In other clinical trials with ketogenic diets, diabetes medications are frequently reduced or eliminated (21, 36–43). The beneficial effects of ketogenic diets for people with type 2 diabetes are attributable primarily to weight loss, with benefits appearing to wane over time (48, 49). Few additional negative impacts on global measures of health have been reported in short-term studies on type 2 diabetes (21, 37, 40). Long-term effects have not been elucidated (49).

Well said.  Nice Find.

  __  Saul

 

[Gordo]

Another study just published explaining how high protein diets may shorten lifespan: https://www.nature.com/articles/s42255-024-00984-2

Edited February 20 by Gordo