Does a healthy ketogenic diet cause irreversible insulin resistance?

(You've tried everything else; why not try bacon?) #262

Just how much carbohydrate our ancestors ate is debatable, but 80 g/day is not necessarily non-ketogenic, if the person is insulin-sensitive.

Isotopic analysis of bones is one way. Dr. Michael Eades has a lecture on “Paleopathology and the Origins of the Paleo Diet,” available on YouTube, in which he discusses this.

Again, isotopic analysis of bone remains is a good indicator. A population eating exclusively meat has to have been in ketosis all the time.

Most primitive societies had a traditional diet that involved eating almost exclusively meat. They regarded plant foods as fit only for eating during times of famine. The more isolated of these tribal societies can certainly be taken as suggestive, even though they are not proper “evidence” of what our ancestors ate. Certainly the experience of the Pima Indians, the Inuit, and the Maasai, among many others, where the transition from the traditional diet to the Western diet has been observed, shows that a diet low in sugar, starches, grains, and other carbohydrates is extremely healthy. George Mann in the 1960’s examined around 400 Maasai and could find no evidence of heart disease, except for one man, whose EKG was inconclusive. An earlier report by the British colonial administration compared the health of the Maasai very favourably to that of their vegetarian neighbours, the Kikuyu, who were not nearly as healthy.

(You've tried everything else; why not try bacon?) #263

Shocking as it may seem, there has been no research that I know of to examine the effect of a ketogenic diet on a man’s testosterone levels* (and probably not on a woman’s, either). After all, a ketogenic diet is unsustainable and will kill us. (Though I’ve never been able to figure out whether it will kill us before or after we become unable to continue eating this way.)

#NOTDEADYET

*or more accurately, the effect of a ketogenic diet on a man’s need for testosterone. @SomeGuy’s post above about how the reference ranges are derived is relevant here.

P.S.—In a post above, I raised the possibility that a man might need less testosterone on a well-formulated ketogenic diet, but it is also perfectly possible, for all we know, that a man might need more. But it hasn’t been studied yet, so we cannot know.

(Joey) #264

Given the unknowns of testosterone & keto, perhaps the relevant question is not whether keto will kill us before or after we become unable to continue eating this way, but whether it will kill us before or after we procreate. :breast_feeding:

(Michael - When reality fails to meet expectations, the problem is not reality.) #265

@fitbod I posted this a couple of other places recently and am doing so again here for anyone who’s interested. Michael Eades covers how we know what our pre-agricutural / paleolithic ancestors ate. It wasn’t plants much. In fact, he cracks a joke about Paranthropus robustus (aka Australopithecine robustus) one of the descendants of A. Afarensis (aka ‘Lucy’) who apparently tried to revert to primarily plant eating. Hint: P. robustus left the pool long ago.

PS: Folks who think our ancestors were not in continuous ketosis or only in ketosis seasonally have the onus to demonstrate what they think our ancestors were eating instead of exclusively fat and meat. Eades touches on this a little in his presentation. Keep in mind that the available ‘carb foods’ during the Pleistocene were very different from the available ‘carb foods’ now. See the following for a fuller discussion:

PPS: This is an updated YouTube on this subject by Eades. I’ve posted the older, original in a few topics as well.

Higher glucose over previous years
(Michael - When reality fails to meet expectations, the problem is not reality.) #266

This is a good and informative read for the layman.

Lots of refs cited and linked.

We came out of the trees not to eat the grass, but to eat the grass eaters!

William Kiltz April 22, 2021

(Michael - When reality fails to meet expectations, the problem is not reality.) #267

Another very interesting read. A little more technical and detailed than my previous link, but still very easy to understand.

(You've tried everything else; why not try bacon?) #268

Since even the SAD doesn’t kill us before we procreate (although impotence, obesity, and PCOS can be obstacles to that goal), it’s not likely that keto will.

The only damage I’ve heard of to children involves the ketogenic diet to treat epileptic seizures, which was formulated to be so high in fat (80-90% of calories) and so low in protein, that it stunted the growth of some patients when they entered puberty (they may also have been trying to keep calories low). It turns out, however, that a more reasonable amount of protein still allows for seizure control. Growing children should not stint on protein, and should be getting enough fat to fuel their growth.

#269

Just got my new labs

image
image.png1110×241 22.6 KB

(Joey) #270

Perhaps this ought to be the start of a separate thread, but I’ll reply here for now…

May I pose two (personal) questions:

1 - Do you happen to be a “healthy nonobese male (BMI<30) between 19 and 39 years old”? If not, see below.

2 - Are you suffering from some combination of these symptoms? …

  • Decreased sex drive
  • Decreased energy
  • Depression
  • Erectile dysfunction
  • Infertility
  • Decrease in hair growth on the face and body
  • Decrease in muscle mass
  • Development of breast tissue
  • Osteoporosis
  • Difficulty concentrating
  • Hot flashes

If not, I would encourage you to stop worrying about (or even bothering to test) your testosterone levels. It’s data that’s irrelevant, non-actionable, and counterproductive to your sense of well-being.

If so, then it’s worth pursuing whether you are indeed suffering from hypogonadism, in which case testosterone replacement therapy might begin to be an option to address such symptoms.

Best wishes!

BTW, The bottom of the “Reference Range” (i.e., 95% of the subject population) for various older age groups of nonobese men in the same study which your lab report cites was found to be:

Age => Bottom of “Reference Range”

40–49 => 235
50–59 => 219
60–69=> 218
70–79=> 218
80–99=> 157

(SunnyNC) #271

I will try it next time I cycle back to Keto. Currently I switched to “slowcarb” which is pretty much carnivore-dairy+beans/lentils. Interestingly eating all the extra carbs in the form of beans and lentils has made no difference in my post meal BG. It’s pretty much the same as pre meal or even lower, similar to Keto. I definitely feel more satiated and full. My avg is trending lower than keto but I need more time to make any conclusions. I am going to do this for another week and back to keto. Will try drinking red wine then, which I love anyway and compare results.

(SunnyNC) #272

I can confirm that A1C while on keto is reliable for me. I know because it corresponds to increasing avg BG and estimated a1c based on CGM. I had posted a screenshot shot of CGM predicted avg BG and A1C. Seems pretty spot on.

(Joey) #273

FWIW, red wine remains my favorite plant food. :wine_glass:

(Michael - When reality fails to meet expectations, the problem is not reality.) #274

Just posted this as a new topic.

(SunnyNC) #275

Kudos for saying this. I have said this several times before but that concern somehow gets lost as the discussion turns to what causes high FBG instead of the potential harm. There are a few that do acknowledge this while believing it’s not a cause for concern. I truly appreciate and respect those comments. Tagging @Corals be as she is one of the very few that share our concern. I read in a diabetes book that the blood stickiness is much higher at 110-120 compared to 70-80. To me it’s seems like it’s common sense that it does not matter WHY the sugar is high if the end result is increasing the stickiness (via glycation). Yes less insulin in good. That’s only one part. The other part is glucose itself. Those quoting Bikman should look up his you tube video from LEVELS company. He is now saying he is not sure if high BG is ok even in fat adapted ketogenic people. He started a clinical trial to study this. Phineys Virta study - dishonest. They stopped publishing a1c results. Links in their website pertaining to high fasting BG while fasting are all now broken. This is a BIG red flag. It’s interesting the only evidence some have is evolution. My opinion is (please don’t ask me for studies, my opinion is worthless anyway), that evolution is optimized for survival of species, not longevity. I am sure some, if not all folks here are more concerned about personal long term health and longevity. Chronic stress, constant need for cortisol to induce GNG to release sugars is ok? IDK but I want to thread on the side of caution and assume that’s not good. I think cyclical KD is what I want to do for now. Till their is more research, to each their own. In the meantime, I appreciate that we can at least debate/discuss and learn what each side of this debate has to say. I am grateful I am learning new interesting thoughts/ science as a result of these forums! Cheers.

(SunnyNC) #276

Beautiful comment! Even though I have ”chosen" (maybe unwisely so) to believe the opposite, I am really fascinated by what you say. I have seen papers that claim a stable low variability is better than wild swings, for a given A1C range. They don’t however talk about - Now if the variability is low, let’s say flat line but higher in pre diabetes range, is it causing an ever so slight damage to toes and limbs? If not now, will it add up over the decades? Slow cooker vs pressure cooker, it’s a matter of time, end result my beef chilli is cooked :slight_smile: and it turns out I could have prevented this by keeping that line lower? Let’s say a very healthy Mediterranean style diet. We have all seen the blue zones longivity argument I am sure. My partners granddad lived to 95 perfectly healthy till the last couple months when he stopped eating when he felt his time had come. He ate meats, grains, legumes and fats every meal. Maybe he was blessed with fantastic genetics. Once again highly anecdotal and a worthless N=1 example but I think that now wants to make me want to be open minded and look into both sides more and very carefully. If someone is diabetic, I don’t have a pinch of doubt keto is the way to go. Some one that is NOT diabetic or epliptic? IDK anymore. I have shared this, perhaps useless, anecdote earlier in this thread- My partner is vegan, but eats fish couple times a month (vegan-pescatarian diet). High carb diet obviously. His TG, LDL, HDL are fantastic. His last A1C was 4.5. He is even in ketosis after over night fasting and skipping breakfast, I made him check once out of curiosity. . My numbers are all good, except the typical high LDL that us Keto folks tend to have. I did NMR which came back excellent. So not worried about LDL anymore. But my darn A1C crept up to 5.7, prediabetes. So why should I blindly assume (for myself only) that Keto is better ( despite becoming pre diabetic ) than, let’s say, healthy pescatarian, unless I have health conditions and allergies, which I currently don’t have any? I am obviously biased towards Keto because of it’s otherwise proven benefits, which I have experienced . So I hope keto is indeed the best for longivity as well! Since there is no research, I welcome any reasonable anecdotal experience. Tagging @Corals, @JustMo

(SunnyNC) #277

They might if they are calorically deficit yet somehow kept a good metabolism going by being active all day long (job that keeps them moving all the time)? I had mentioned this earlier, my partner on high carb can get into ketosis after overnight fasting. Definitely not SAD though. More of a vegan/pescatarian Mediterranean type diet. Definitely eats a couple of heavenly hunk cookies everyday, which was my GOTO treat prior to keto. I suspect he’s in calorie deficit as he walks all day long at the hospital where he works.

(You've tried everything else; why not try bacon?) #278

You can’t out-exercise a poor diet. Even 20 g/day of carbohydrate is more than the amount the body likes to keep in circulation, which amounts to about a U.S. teaspoon. Given that the liver makes glucose in the absence of dietary glucose, carbohydrate is actually not necessary in the diet at all. There are no known carbohydrate deficiency diseases, whereas the consequences of failing to ingest the necessary quantity of essential amino acids and essential fatty acids are well known.

(SunnyNC) #279

Great points, once again Joey. I also wonder, at what point the benefit tips, ie some fluctuation but with lower averages is desirable over low variability but higher average… someone thats always between 135-140 cannot be better than someone that fluctuates from 70 to 140 but stays below 90 most of the time?? Most of the blood glucose studies are on diabetics and not on healthy individual due to the way funding is obtained. So I don’t think we’ll have any answers anytime soon. I hope Bikman is able to fund and conclude the levels study.

Doesn’t the burden of proof actually fall on the opposite? I mean we can all agree, for someone eating SAD, higher fasting and higher avg is generally bad. So then, is it ok on Keto, if so why? No studies means safe assumption is to lower BG till studies prove otherwise. I know all your other measurements are fine, I am just trying to, in a friendly manner, challenge why the burden of proof should be other way around like you and many others claim! :slight_smile: If you don’t know all the pro/cons, then don’t do it (safety prioritized) Vs if you don’t know all pro/cons, do it anyway (take risk but might benefit).

Nobody here is. If you read the comments the concern is about increasing A1C

(Joey) #280

I’ve thoroughly enjoyed the exchange throughout this thread. But I’m afraid you may still be ceding the point to the Western/SAD diet “standard-of-care” trap.

Plenty of peer-reviewed research supports the conclusion that, while high HbA1c levels are strongly correlated with “known diabetics,” HbA1c is a rather poor diagnostic tool when applied to non-diabetics.

So, are we diabetic? prediabetic? struggling with metabolic syndrome?

That’s where the Oral Glucose Tolerance Test (OGTT) comes in.

Because the OGTT actually reveals the maximal glucose level before the insulin response effect kicks in. And it’s the maximal glucose level that causes the tissue damage associated with diabetes.

Someone who is alive is both inhaling and exhaling in equal volume. Based on volume/direction of airflow, on average, they’re not breathing at all. Such an average may be mathematically correct - but it’s not a good diagnostic tool.

In terms of human reproduction, there are two sexes. On average, we humans have roughly one testicle and one ovary. On a population-wide basis, these averages are accurate enough. But individual context is everything.

An HbA1c of 5.0% translates to an average glucose level of 97 mg/dL.

That 5.0% average might be the result of swings up to 200 mg/dL (diabetic), or perhaps only as high as 130 mg/dL (perfectly normal).

Context is everything. How often do they eat? How quickly is insulin released? How responsive are the insulin-sensitive tissues? How quickly does their glucose come down? And, of course, what are they eating?

The metabolic health of two individuals with identical HbA1c measures could be the difference between night and day.

When testing patients eating standard SAD who present with certain clinical signs of metabolic syndrome, the standard-of-care use of an HbA1c measure (with a reference range based on that large population who eat western SAD) for assessing risk of diabetes may be imperfect, but still somewhat useful as a first screen tool. Then an OGTT would be a logical next step to see what’s really going on.

For those who are not eating meaningful quantities of dietary glucose, I have a hard time imagining how an (assumed) 3-month average blood glucose figure can reveal much about the fasted vs post-prandial excursions of glucose and insulin in those who refrain from the SAD WOE.

Same points. Put differently? :vulcan_salute:

(You've tried everything else; why not try bacon?) #281

No, I don’t think so. The fact is that the bodily mechanisms regulating serum glucose evolved over two million years of a low-carbohydrate, high-fat diet (at least, according to radioisotope analysis of the bones found at archaeological digs). So it is more reasonable to assume that if someone’s glucose is higher than expected on a ketogenic diet, there is a strong possibility that’s not a problem. Note that I say possibility, because we have no data to argue either way.

Now, it is entirely possible that you have a genetic mutation that makes serum glucose over 100 deadly to you, so perhaps you are indeed right to be concerned, I don’t know. Myself, given what I have learned over the past five years on a ketogenic diet, I choose not to be so concerned—at least, given the absence of data.