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paulgfoster

macro nutrient ratios

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I have been managing very well to adhere to my allocated calories of late but must admit to total confusion over macro nutrient ratios..........The more i read the more i am not sure,  I read Ornish Pritikin and it sounds plausible.....i was on Pritikin for years and scored zero on the coronary calcium scan,..........

Then i ate sad and moved towards metabolic syndrome..........cr has fixed this , but how should i eat now........

There is a huge movement towards high fat and olive oil, and it all makes sense...........I dont feel happy with a Paleo approach as i dont eat meat anyway.............ON a strict  low fat regime like Pritikin i will have low cholesterol and ldl but also very low Hdl............some say this is risky , Pritikin says it isnt and higher fat diets which in my case would lead to  better hdl levels,  lead to more arterial plaque.   

Whatever is thought about recent changes in attitudes to fat if Ancel Keys practiced what he preached he did live to a 100.

At the moment i have increased my fat intake to 50% of calories, and although mostly healthy fats my sat fats go up to nearly 20g a day along with them.

I dont eat refined carbs at all or sugar, no bread, rice pasta or potatoes.

Part of me says go back Ornish ?pritikin and the other part just doesnt know, and the more i read the more it seems the scientific community doesnt know either.(conclusively)

What sort of macro nutrient ratios do most others follow on here?

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I follow mostly 15% Protein, 35% Fats and 50% carbs.  Once I balanced out my fatty acid intake (5:1 ratio or less) and fat consumption, my cholesterol numbers went from bad to good. My saturated fats are around 10 g per day and cholesterol intake is < 200 mg.  I eat mostly vegan.  I brought my HDL from 27 up to 58 or so and I'm quite happy with that. 

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I'm glad someone stepped in to answer you, Paul :) . I suspect there is some reluctance to weigh in on this on the part of long-time CR Society members because these issues have been hotly debated for decades now (literally), and nothing has ever really been resolved — and, of course, a few times a year a newcomer pops in convinced that hir approach is correct, and that we can't possibly be familiar with the incredible body of knowledge that s/he has accumulated on the subject from reading Gary Taubes or articles on the internet ;) .
 
In the early days of the CR Society, most people were still under the sway of the very low-fat dogma that was predominant in nutrition advice of the time, and that was advanced by none less than Dr. Walford in his books, and championed by several members who were quite active on the Listserv, such as Ben Best. I personally think this is very unwise (more on this below). One thing that came up a lot at the time as a result was constipation (see discussion here).
 
Around the time that I joined the Society back in 1999, the Society made a pretty big transition into the Zone macronutrient profile, which is often said to be a 30:40:30 P:C:F but actually involves determining your protein needs (by Zone standards of 1 g/kg body mass), then calculating a P:C of 0.75, then making up the rest of one's Caloric target with fat. One can then further tweak one's ratios by adjustment according to subjective & objective responses to the meal (see Mastering the Zone for the former, or The Anti-Aging Zone for the more complete list, including the full "stool evaluation" referenced in the just-linked discussion of the low-fat constipation problem). The Zone diet itself had been quite the rage in the relatively recent past, and several people (of whom Sherm (Michael Sherman)) and I were the most active) advocated in favor of it extensively on the Listserv.
 
A poll of CR Society members' macronutrient balances done back in 2001 revealed a wide range of macronutrient choices, but that a Zonish macronutrient cluster that seemed to make up the largest portion.
 
As Dean P. said at the time,
 

Based on 38 people responding, my (potentially biased) interpretation is that a Zone-ish diet seems to be favored among the respondents. The interpolated "peak" of responses for the three macronutrients are:
 
Carbohydrates: ~41% Protein: ~25% Fat: ~32%
 
Interestingly, there appears to be a definite spike of "Walfordians" in the 61+% carbohydrate range (10 out of 38 respondents = 26%).

 
38 respondents is of course a tiny fraction of the List membership, and they were self-selected; also, this was in the recent wake of fairly vigorous promotion of the Zone by Sherm and me, and indeed the relatively recent publication of the Zone books prob meant that a significant # of people prob got interested in CR after reading them.
 
That said, I suspect that this survey was still pretty representive, and may still be. The WUSTL study (1,2) reported (albeit again in a small, largely self-selected group -- but NB that by definition they were long-term, successful CR folks at substantial %CR) that their subjects consumed "~26% of calories from protein, ~28% from fat, and ~46% from complex carbohydrates". 
 
The next big move was in reaction to Dr. Fontana's discovery that such modestly high intakes of protein could block the effects of CR on IGF-1 in humans, and the move (which I eventually joined) to cut back protein quantity and quality sufficiently to bring IGF-1 levels down to low-normal; see my discussion of protein in the CR diet, which includes a link to alert you to the complicating factor of vegetarian/vegan protein sources and IGF-1 in the CR diet.
 
More recently, we've had a fair number of people come aboard practicing and/or advocating for very-low-carb Atkins-type diets, either full-on ketogenic or nearly so.
 
I personally have, in the course of my >15 y of CR tweaking, varied from 15-35% protein at each meal, never let myself go below 30% fat, and made up the remainder in carb accordingly. I am currently at 20:38:38 P:C:F plus ≈4% alcohol from red wine. I have a really hard time getting my IGF-1 levels to stay low-normal, as opposed to sky-high or too-damned-low. I keep my fat between 30-38%, and adjust my carb accordingly.
 
On Esselsyn/Ornish/Pritikin/McDougall: the studies purported to support the ultra-low-fat approach are not worth the paper on which they're written (to the extent that anyone keeps hardcopies any more). Esselsyn's and Ornish's  reports are in very small numbers of intensely-managed patients with existing CVD; neither of them have reported any actual improvement in survivorship; and there are major confounders for both. Esselstyn is reporting a case series from his personal practice, and not (as is often claimed) a clinical trial: there was no control group, and moreover ALL of his subjects were on cholesterol-lowering drugs.(3) The benefits reported for Ornish's program are not demonstrably related to the diet, let alone demonstrably better than a diet higher in quality fat: his intervention not only included lower saturated fat intake (which is of course achievable with a diet high in mono- and polyunsaturated fats), but also a "vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support" (4), none of which were administered to the controls.
 
In any case, I think the main thing to remember is that pretty much everyone recognizes that these are actually really rather marginal, tweaking issues next to the incredibly powerful effects of CR itself on anything that macronutrient manipulation might meaningfully affect.
 
-Michael
 
1. Fontana L, Meyer TE, Klein S, Holloszy JO. Related Articles, Links Free in PMC Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6659-63. Epub 2004 Apr 19. PMID: 15096581 [PubMed - indexed for MEDLINE]
 
2. Meyer TE, Kovacs SJ, Ehsani AA, Klein S, Holloszy JO, Fontana L. Related Articles, Links Abstract Long-term caloric restriction ameliorates the decline in diastolic function in humans. J Am Coll Cardiol. 2006 Jan 17;47(2):398-402. PMID: 16412867 [PubMed - indexed for MEDLINE]
 
3. Esselstyn CB Jr. Related Articles, Links Abstract Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am J Cardiol. 1999 Aug 1;84(3):339-41, A8. PMID: 10496449 [PubMed - indexed for MEDLINE]
 
4. Ornish D, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ. Related Articles, Links Free Full Text Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998 Dec 16;280(23):2001-7. Erratum in: JAMA 1999 Apr 21;281(15):1380. PMID: 9863851 [PubMed - indexed for MEDLINE]

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Thank you for the replies Keith and Michael, they are very much appreciated. I am at the moment about 16/40/40  and 4% alcohol for my 100ml glass of red wine............when i tried to increase fat levels i did not feel as well and had less energy when exercising.  Also unhappy about increasing sfa levels, so will probably stay at my current ratio which seems to work best for me.  It is always re assuring to know what others are doing, especially those that have been practicing some time............

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I have personally never had a diet more than 15% protein.  That's what I have currently only because I'm deliberately losing weight at a pretty rapid clip.  When I transition, I'll cut back to 10-12.5% protein...still higher than I used to do, but far more will be plant-based and much less meat, with regards to methionine restriction.  I'm playing with the idea of glycine supplementation.  Straight gelatine is fabulous in Indian-style lentil soups and curries--don't even notice it.  It's revolting in yogurt.  I'm hoping straight glycine will work in yogurt.  I really like it.  :)

 

Overall, I used to eat about 8% protein, 10% fat, 82% carbs, probably half the bad kind.  I wasn't consciously controlling fat or protein.  I just like carbs.

 

I will be eating 10-12.5% protein (7% or less from animal sources), 20% fat, and the remainder carbs, with only one once a day refined max and/or only 2 teaspoons added sugar across all foods max.  (Added sugar's easy.  Refined is a sacrifice.)

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On 5/1/2015 at 10:49 PM, paulgfoster said:

Thank you for the replies Keith and Michael, they are very much appreciated. I am at the moment about 16/40/40  and 4% alcohol for my 100ml glass of red wine............when i tried to increase fat levels i did not feel as well and had less energy when exercising.  Also unhappy about increasing sfa levels, so will probably stay at my current ratio which seems to work best for me.  It is always re assuring to know what others are doing, especially those that have been practicing some time............

Yes Paul a high fat meal will make on quite sluggish when exercising. Please keep in mind that olive oil is 14% saturated fat which just about every serious and trustworthy medical institution recognizes as not a desirable dietary component

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But, again, we may leave the judgment to the lipids panels. If APOB is low and trigs are low, then even if we are eating 2 pounds of lard per day that is not affecting us.

We may also have a calcium score determined as an additional check.

Low-fat, moderate protein, means high carbs. I wonder what happens to blood sugar concentrations with that. Are we swapping CVD risk with the risk of diabetes?

Before trying, I would like to see some serious literature, not just anecdotal or semi-anecdotal reports.

Edited by mccoy

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2 hours ago, mccoy said:

Are we swapping CVD risk with the risk of diabetes?

CVD and diabetes are highly correlated.  People with diabetes have been found 2 to 4 times more likely than those without to die from CVD and stroke.   And studies have shown the risk for heart diseases increases with prediabetes and a very large percentage of seniors are prediabetic.

from https://denversdietdoctor.com/diabetes-vascular-disease-joseph-r-kraft-md/

Quote

To quote pathologist Dr. Joseph R. Kraft, MD, MS, FCAP, the father of the insulin assay:

Those with cardiovascular disease not identified with diabetes… are simply undiagnosed.

One of Dr. Kraft’s conclusions, based on his illustrious career, is simple and provides a profound and ultimate truth: diabetes is a vascular disease. His career spanned decades and included unparalleled research performing insulin assays in over 14,000 subjects, thousands of autopsies, and collaboration with others medical experts searching for the root causes of chronic diseases including vascular disease. He also wrote a book about his research titled Diabetes Epidemic & You.

Here's Dr. Kraft's book http://library.lol/main/4AF10CA01FB106015F677C70605FD20D

 

The glycocalyx may partly explain the correlation.

Quote

Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that cause atheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then causes atherothrombosis.

 And studies have shown an intact glycocalyx is an effective barrier keeping LDL out of contact with the endothelium.

Edited by Todd Allen

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Todd, yes, that's about what I meant, exchanging one kind of CVD for another is not an optimization. By the way, I take it you are following a high fat, low carb or keto diet, what's your strategy to avoid atherogenic risk? Are you able to avoid an elevated ApoB , high inflammation and unfavourable calcium score?

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7 hours ago, mccoy said:

Todd, yes, that's about what I meant, exchanging one kind of CVD for another is not an optimization. By the way, I take it you are following a high fat, low carb or keto diet, what's your strategy to avoid atherogenic risk?

For roughly 4 years I've been eating a ketogenic diet with a lot of experimentation with foods and eating patterns.  I'm guided more by how I feel and perform day by day than optimizing potential biomarkers of longevity.

Twenty years ago I went to my first Kennedy's Disease Association conference and made friends among people who shared the disease and the desire to live with it as best as possible.  We were all partial toward prevailing ideas of healthful lifestyle.  Most have died but a couple linger on in poor shape.  Five years ago I was in terrible health declining rapidly feeling I might die with the next flu or a bad cold.  I was prompted to start making big changes by the abrupt death by stroke of someone unrelated who I joked was my identical twin.  I alternated between fear of death and fear of living with an ever bleaker future.  Much of what I'm doing now is nearly the opposite of what I was doing then and I've regained more health, fitness and zest for life than I thought possible.  I'm hopeful for a long bright future and even if cut down early by heart attack or cancer I'll still feel I've been fortunate.

The lifestyle changes making dramatic positive impacts on my health and fitness appear to also be causing my cholesterol and testosterone to rise.  HDL, LDL and T both total and free have all more than doubled and were still recently rising.  Last month my HDL was 86 mg/dL and LDL was 235 mg/dL.  Here's my T:

T_quest.jpg.5199d1e8b3ffacbb3c0aa168ed3688d9.jpg

Their inverse correlations to my body fat % have been pretty tight and if I make it to a goal of 10% body fat I predict I'll plateau around HDL 100, LDL 350 and T 2700.

My disease is caused by a mutation of the androgen receptor and the evidence that T is essential to the pathology is much stronger than the evidence of LDL being essential to CVD.  I speculate though that T and LDL are not sufficient and solely causal for the pathologies and when enough other things are going well there is little to no disease.  Cholesterol and T both have identified positive effects from which I appear to benefit.  I've been doing things which might raise them higher to see if I continue to thrive despite the risk to crash and burn.

My doctors have begun grudgingly admitting my gains in health despite having no prescriptions and my contrary lifestyle choices.  They still have concern the things I'm doing and some of my numbers might be dangerous.  In addition to high cholesterol and T I've also raised IGF-1 and albumin unusually high and my urine PH has been pegged at the bottom of the reference range for acidity.  To humor them and possibily learn things of value I've been through extensive medical testing.  My primary care doc believes I should be at high risk for heart failure, liver failure, kidney failure and cancer and almost seems annoyed of being unable to produce evidence of trouble.  I do have anomalies.  Very high adipic, malic, isocitric, 5-OH-indoleacetic and BHB acids as well as taurine, serine, beta-alanine, urea and a few other things I don't remember.  On a tread mill my heart rate rises much higher than expected.  But heart structure, rhythm, stroke volume, ejection fraction, blood pressure, recovery and resting pulse as well as all markers of inflammation have improved and are now all good to excellent.  My interpretation is my disease compromises skeletal muscle mitochondrial function and the rest of my body is rising to the challenge up regulating energy pathways such as the Cori and Cahill cycles.

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Todd, your individual situation seems to be far more complex than the average individual, so we can hardly say it can be taken as an example for everyone. In your case, a keto diet has brought about elevated cholesterol levels, specifically high LDL-C, which, for the average individual, raises the risk of atherogenic disease. In your case, I understand high LDL-C may trigger some pathways which are more favourable than unfavorable although, as you say, the balance is a tricky one.

In my personal instance, an LDL-C higher than 100 or 120 would start making em nervous.

 

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20 hours ago, mccoy said:

In my personal instance, an LDL-C higher than 100 or 120 would start making em nervous.

The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression

Quote

If the hypothesis is true that LDL is the driving force of atherosclerosis, one might expect to find statistically and clinically meaningful correlations between LDL cholesterol levels and the extent and progression of atherosclerosis as measured by coronary artery plaque. The same would be expected for TC, which is generally regarded as an adequate surrogate for LDL. Extensive evidence, mostly based on LDL, suggests otherwise. Studies in fact give rise to a set of rather inconvenient questions. Thus if the hypothesis is true one can ask:

  • Why do autopsy studies of the correlation between the extent of coronary atherosclerosis and serum cholesterol yield null results? The answer that the blood samples, mostly from accident or suicide victims, were obtained too long after death has been discredited, and there appears to be no reason to suspect that these studies were carried out either incompetently and with selection bias [5].
  • Why did Hecht et al. [6] find that total TC, LDL, and HDL cholesterol did not correlate with either the extent or prematurely of calcified plaque burden in 1105 consecutive, asymptomatic individuals self-referred for EBT?
  • Why did Hecht et al. [7] fail to find no correlation between LDL and the coronary calcium percentile (correlation coefficient 0.06 with a scatter plot showing no visible correlation) for 304 asymptomatic women? In fact, they found no correlation between either the calcium percentile or score and any lipid measurement.
  • Why when 1653 men and women without a history of CHD were subjected to coronary CT angiography using contrast media did Johnson et al. [8] fail to find a correlation between total plaque burden (calcified, mixed and non-calcified) and total serum cholesterol (Spearman’s rho = 0.04), a result the authors indicate agreed with other studies?
  • Why in a study of the impact of psychosocial factors on coronary calcification in a large group of male and female asymptomatic individuals (n = 780), was there no correlation between TC or LDL and the calcium score with Spearman correlation coefficients near zero? Multivariate analysis gave an odds ratio of 1.005 for LDL [9].
  • Why did Arad et al. [10] in the St. Francis Heart Study find no correlation (r = 0.03, p = 0.15) between LDL levels and coronary calcium scores in 4903 asymptomatic individuals?
  • Why for adults with familial hypercholesterolemia, did Jensen et al. [11] find that age-adjusted coronary calcium scores were not associated with cholesterol levels as assessed by either scatter plots or correlation coefficients?
  • Why did Kronmal et al. [12] find among approximately 2900 individuals that the relative risk of incident coronary artery calcium associated with LDL was only 1.03 per 10 mg/dL and barely reached statistical significance (lower CI 1.01) whereas both HDL and triglycerides exhibited much stronger associations?
  • Why did Sung et al. [13] in a recent study of coronary calcium scores and estimated coronary risk (Framingham), find negligible correlation between LDL or TC and calcium scores in 1653 asymptomatic individuals judged free of CHD (Spearman’s coefficient = 0.07 and 0.08, respectively). Even the correlation coefficient of 0.26 found for the log calcium score vs. 10 year absolute risk estimate yielded a scatter plot suggesting that this magnitude of correlation, which was three to four times greater than that found for LDL and TC, had no clinical utility.
  • Why in a study of 177 asymptomatic patients of intermediate risk of CHD did Ramadan et al. [14] find a null result (OR = 1.022, p = 0.361) for the odds of positive coronary calcification outcome and LDL in a multivariate model? The group studied had a wide range of both LDL levels and calcium scores.
  • Why were Takamiya et al. [15] unable to find any association whatsoever between LDL and coronary calcium in three multiple logistic regression models when 100 asymptomatic individuals underwent EBT.
  • Why do studies that looked for a correlation between TC or LDL and the progression of atherosclerosis find no statistically significant association [12,16–24]? All 10 studies involved EBT. Lack of association was indicated by absence from multivariate analysis or absence or non-significant association in comparisons of progression vs. no progression, or non-significant results in univariate or multivariate analysis. Most studies examined the correlation with LDL as well as TC.

 

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Todd, in my country a direct link to sci-hub will be blocked, so I could not open the link. Right now I agree to disagree, taking as a reference Dr. Tom Dayspring and the latest Dr. Peter Attia. They sure are not a part of the low-fat vegan narartive.

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Well all I know is that when someone inherent a gene that causes very high ldl levels the death rate from atherosclerosis skyrockets and often happens at very young ages. The more severe the levels of ldl the younger they die. Many in their twenties. It’s called familial hypercholesterolemia.I  have it. My twin daughters have it also. Ldl levels over 200 in my family. Many died young including my father. The research I’m reading from Cleveland clinic, Harvard etc. claim  no atherosclerosis when populations have ldl levels drop below 70. I won’t bother to look it up cause people believe what they want to believe. I would love to believe that ldl doesn’t matter and I’d love to see the proof. In the meantime I’ll take my 40 mg of Crestor and glad, so glad my dear daughters are taking statins!

Edited by Mike41

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33 minutes ago, Mike41 said:

Well all I know is that when someone inherent a gene that causes very high ldl levels the death rate from atherosclerosis skyrockets and often happens at very young ages.

There are a bunch of genes that contribute to FH and it comes in many flavors.  Some have exceptionally high LDL and no heart disease and excellent longevity.  Other things have been found to correlate much better than LDL to early death from FH such as ferritin, homocysteine, clotting factors, markers of inflammation, etc.  If your flavor of FH comes without any other high risk factors sweating over LDL might be unwarranted.

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1 hour ago, mccoy said:

Right now I agree to disagree, taking as a reference Dr. Tom Dayspring and the latest Dr. Peter Attia.

I listened to it too.  I think an oversight on their part was to not acknowledge that something like 88% of adults in the US (and most other westernized countries aren't too far behind) are insulin resistant with chronic hyperinsulinemia.  A marker of this the triglycerides to HDL ratio.  Numerous studies have shown that when this ratio is bad (>4) there is a significant correlation between LDL and CVD but when the ratio is good (<2) the relationship disappears.  My ratio has dropped to ~0.8.

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Global associations between macronutrient supply and age-specific mortality

From the abstract, a seemingly very high calorie recommendation.

Energy supplied at around 3,500 kcal/cap/d minimized mortality across ages. However, we show that the macronutrient composition of energy supply that minimizes mortality varies with age. 

The recommendations for young and old:

In early life, 40 to 45% energy from each of fat and carbohydrate and 16% from protein minimizes mortality. In later life, replacing fat with carbohydrates to around 65% of total energy and reducing protein to 11% is associated with the lowest level of mortality.

The authors comment on the Okinawan diet:

He does note that a traditional Okinawan diet is low in protein — at around 9 percent — but is higher in carbs — 85 percent — and much lower in fat — 6 percent. There’s also an Okinawan elder’s diet that “gets a bit closer in the carb and fat dimensions” — hitting a respective 58 and 26 percent — but it's higher in protein at 16 percent.

I think I'd like to see this article confirmed by other studies.

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19 minutes ago, corybroo said:

I think I'd like to see this article confirmed by other studies.

Also from the abstract:

Quote

Animal experiments have demonstrated that energy intake and the balance of macronutrients determine life span and patterns of age-specific mortality (ASM). Similar effects have also been detected in epidemiological studies in humans. Using global supply data and 1,879 life tables from 103 countries, we test for these effects at a macrolevel: between the nutrient supplies of nations and their patterns of ASM.

They aren't actually testing anything.  They are finding a correlation at a very coarse level.  Additional observational studies confirming the correlation still wouldn't confirm causality.

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On 11/15/2020 at 1:16 PM, Todd Allen said:

The lifestyle changes making dramatic positive impacts on my health and fitness appear to also be causing my cholesterol and testosterone to rise.  HDL, LDL and T both total and free have all more than doubled and were still recently rising.  Last month my HDL was 86 mg/dL and LDL was 235 mg/dL.  Here's my T:

T_quest.jpg.5199d1e8b3ffacbb3c0aa168ed3688d9.jpg

Their inverse correlations to my body fat % have been pretty tight and if I make it to a goal of 10% body fat I predict I'll plateau around HDL 100, LDL 350 and T 2700.

I'm not going to lie, when I saw these numbers my jaw pretty much hit the floor. Having said that, I have no idea what it would be like to live with your particular condition and I very much appreciate your willingness to experiment and make up your own mind about what's best for you. The last time I had my cholesterol checked my total was 117, which would come back at roughly a quarter of your 100+350 goal. That T level is also the highest natural level I have ever seen. I would be curious to see a more detailed breakdown of your hormonal panel if you had one available and are willing to share. Your levels starkly contrast many people's experiences on this board as CR often involves a reduction in T levels, though not everyone experiences this. 

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17 hours ago, Todd Allen said:

There are a bunch of genes that contribute to FH and it comes in many flavors.  Some have exceptionally high LDL and no heart disease and excellent longevity.  Other things have been found to correlate much better than LDL to early death from FH such as ferritin, homocysteine, clotting factors, markers of inflammation, etc.  If your flavor of FH comes without any other high risk factors sweating over LDL might be unwarranted.

All I can say for me, my brother and numerous cousins we didn’t succumb. Many died in their forties. Uncles, grandfather, great uncles. What was the one difference?  statins! btw the research on numerous victims of FH show similar results. That said I will agree that LDL is not by any means the only part of the puzzle. Another important lipid factor is triglyceride/Hdl ratio. Lower than two is desirable. And there is The Who LPA and density of ldl issues. These complexities along with the apparent genetic invincibility some folks have to atherosclerosis even when they break all the rules, insulin resistance, smoking, high BP, etc. may likely explain the paradoxes of high ldl and no atherosclerosis.

Edited by Mike41

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On 11/17/2020 at 8:33 PM, drewab said:

The last time I had my cholesterol checked my total was 117, which would come back at roughly a quarter of your 100+350 goal.

Mine isn't so much a goal but just a rough estimate of where I expect to plateau.  Here's a plot from a survey article at CholesterolCode suggesting my numbers are fairly average for people eating keto.

HDL_LDL_plot.png.be71a0eda02a6396230b23e4b5940644.png

It appears only the lean and athletic get LDL up in the 400-600 range.  The highest I know of (without FH) is a woman who reported LDL labs in the mid 700s but she does power lifting competitions at single digit body fat % and I think was eating a beef only diet.  Her LDL was 80 when her sport was running and she was chubby and eating high carb.  Here a video interview with her back when her LDL was in the 400s. 

 

On 11/17/2020 at 8:33 PM, drewab said:

That T level is also the highest natural level I have ever seen. I would be curious to see a more detailed breakdown of your hormonal panel if you had one available and are willing to share.

I think my high T is due to the expanded CAG repeat mutation of the androgen receptor gene which causes my disease SBMA.  In clinical exams it is typically distinguished from ALS due to also causing signs of androgen insensitivity such as gynecomastia.  I believe androgen receptor activation has a counter regulatory role on testosterone production.  People with early stage SBMA still in good health tend to have mildly elevated T although it drops as the disease advances probably due to declining metabolic health.  The first clinical trial of a drug therapy for SBMA was of testosterone supplementation and it accelerated neurodegeneration.  I'm hoping my rising natural T in a context of improving health won't be as problematic.  My gynecomastia is mostly gone and I am even growing some hair on my chest suggesting my body has found a level that compensates for the androgen insensitivity.  A possible downside is that people with SBMA have low risk of prostate cancer and I might lose that benefit especially as I am trying hard to maximize IGF-1 with some success.

I only had a few other hormone labs most recently:

DHEA-SULFATE  195 mcg/dL   38 - 313

IGF-1  321 ng/mL   40 - 290

TSH    1.35 mIU/L    0.40 - 4.50 mIU/L

and some consider this a hormone

VIT D 25-OH TOTAL    57 ng/mL    30 - 100

 

Edited by Todd Allen

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On 11/17/2020 at 11:11 PM, Todd Allen said:

I listened to it too.  I think an oversight on their part was to not acknowledge that something like 88% of adults in the US (and most other westernized countries aren't too far behind) are insulin resistant with chronic hyperinsulinemia.  A marker of this the triglycerides to HDL ratio.  Numerous studies have shown that when this ratio is bad (>4) there is a significant correlation between LDL and CVD but when the ratio is good (<2) the relationship disappears.  My ratio has dropped to ~0.8.

Todd, I don't know those studies so I cannot give you an answer, but until they are going to become a recognized part of preventive medicine, I would prefer not to gamble. Call me overcautious. 

I also find strange that Peter Attia's team, made up of 5 people exclusively dedicated to reading all literature related to everything about risk prevention did not intercept those studies. If anyone of us is a member of his plan, it would be a good question to pose in one of his AMAs.

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