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The thread on keto (and low carb) diet


mccoy

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Dr. Baker was a orthopedic surgeon not a cardiologist.  You're okay with an LDL of 287? Fantastic!  I was not okay with an LDL of 130 and neither was my cardiologist for the fact I have a brother who had a bypass about two years older than I am now who had lower LDL than I had.  My LDL is now 60 with a total cholesterol of 148, HDL of 77 VLDL of 11 and triglycerides of 53.   I had A-fib and after 3 ablations I have been back in normal rhythm for over a year.  My brother is now 80 and the oldest male in my family ever.  

I was not okay with A-fib, not okay with high LDL and was very okay with getting my two shots of vaccine.  I am not joining the "Death Cult"   I had said it before that I wasn't posting to this site anymore and probably will stop reading it.  I turn 72 in a few days and have no time for nonsense that only angers me.  

Live and be well.   

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7 hours ago, pete533 said:

Dr. Baker was a orthopedic surgeon not a cardiologist.

You are right, my bad.  I actually don't follow Dr. Baker much as I have no interest in going full carnivore and I'm not sure why I assumed he was a cardiologist.  It was the keto cardiologists Dr. Bret Scher and Dr. Aseem Malhotra who instigated my questioning of LDL as a risk factor for the healthy and lead me to be comfortable with my rising cholesterol.  But if I had A-fib and a family history of heart disease I'd probably be less inclined to let go of that fear.

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2 hours ago, pete533 said:

Maybe you should have your arteries checked for plaque periodically to be on the safe side.  You know, "Trust but verify"

My primary care doc is concerned about the potential CVD risk of my high cholesterol and my endocrinologist is concerned about the potential CVD risk of my high T, DHT and estradiol.  I'll continue with recommended testing but so far I'm pleased with my results.  There are other keto supportive cardiologists such as Dr. Nadir Ali and Dr. Ethan Weiss that contribute to my comfort with the path I'm on.  None actually say high LDL does not matter but all seem to agree there isn't significant data on the risk of LDL in the absence of other risk factors such as hypertension, hyperglycemia, high triglycerides, low HDL, high fibrinogen, high homocysteine, inflammation, oxidation, pattern B LDL, etc.  I don't have those risk factors and I don't have indications of CVD and I have compelling reasons for the path I have taken.  It isn't denialism but my personal risk/benefit calculation based on imperfect info much like the choices I make among financial investments.  Regular reappraisal to correct mistakes while small is about the best I hope for.

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On 8/10/2021 at 6:22 PM, Todd Allen said:

My primary care doc is concerned about the potential CVD risk of my high cholesterol and my endocrinologist is concerned about the potential CVD risk of my high T, DHT and estradiol.  I'll continue with recommended testing but so far I'm pleased with my results.  There are other keto supportive cardiologists such as Dr. Nadir Ali and Dr. Ethan Weiss that contribute to my comfort with the path I'm on.  None actually say high LDL does not matter but all seem to agree there isn't significant data on the risk of LDL in the absence of other risk factors such as hypertension, hyperglycemia, high triglycerides, low HDL, high fibrinogen, high homocysteine, inflammation, oxidation, pattern B LDL, etc.  I don't have those risk factors and I don't have indications of CVD and I have compelling reasons for the path I have taken.  It isn't denialism but my personal risk/benefit calculation based on imperfect info much like the choices I make among financial investments.  Regular reappraisal to correct mistakes while small is about the best I hope for.

LDL Cholesterol – Ron Krauss MD | Me and My Diabetes

What do you think about those that say paying attention to the type of LDL is the most important thing to consider in terms of risk factors -- 

"The simplest way to describe it is as large and small. These are cholesterol containing balls of fat that come in different sizes. And the larger forms of LDL carry cholesterol but they don’t seem to do as much damage to the arteries as the smaller LDL particle."

"Dietary cholesterol coming in eggs and shellfish has modest effects on cholesterol. It’s much more effected by the type of fat and carbohydrate. The fat that causes LDL to go up is saturated fat. Animal fat. We’ve shown that it tends to affect the larger LDL, interestingly. What we tend to think of as bad fat primarily affects the less bad form of LDL, whereas carbohydrates, in a somewhat counterintuitive way, it’s starches and sugars that raise the bad form of LDL."

Any thoughts on these statements?>

 

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6 hours ago, alexthegra8 said:

What do you think about those that say paying attention to the type of LDL is the most important thing to consider in terms of risk factors

I think the evidence is fairly compelling that LDL cholesterol as reported on standard lipid panels is only weakly correlated with CVD risk.  Other measures such as OxLDL, particle size distributions, ratio of LDL-C to particle count or ApoB, Lp(a), triglycerides to HDL ratio, etc. appear to be better indicators of risk.  I haven't seen consensus on any one test being the most important thing to consider.

I've had large increases in cholesterol as I've increased intake of saturated fat both with coconut oil and animal fats.  But at the same time as LDL-C has gone up HDL is up, triglycerides are down, OxLDL and makers of inflammation are low and falling, and NMR lipoprotein profile looks excellent.  I do not know how to judge all of these results together but my base heart rate and blood pressure are good and under extreme exertion I have no sense of cardiac insufficiency or trouble and tests such as EKG, ECG, CT, etc. don't show any disease.  I know heart disease is considered a silent killer but I think that is mostly due to not paying attention.  I'm willing to bet that if I am paying close attention and getting thorough medical exams and testing the risk of a heart attack sneaking up and killing me without warning is minimal.  And if it does, so be it.  There are worse ways to die.

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I saw a video from the same Mike the Vegan, where he was measuring his fasting glucose with a strip glucometer. His FBG was 115 mg/dL, and he said it was probably due to the bananas he ate the night before.

He's a young guy, but at least in that instance, his status was the same as that of a prediabetic.

I'd like to see measurements of FBG in people following a lowfat, hi carbs diet. Dean posted a link to one study, but the diet was slightly hypocaloric and very strict: vegetables, cereals and sesame is all they ate. Such kind of diet appeared to provide low blood glucose and low lipids. But not everyone would be able to follow it. I would probably not.

Edited by mccoy
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https://www.sciencedaily.com/releases/2019/08/190813080206.htm

IgA is naturally produced by our bodies and is crucial to regulating the bacteria that live in our gut. It acts as a defense mechanism that helps neutralize potentially dangerous bacteria that take advantage of changes to the environment, such as when we consume an imbalanced or fatty diet,

In their experiments, they also observed that IgA deficient pre-clinical models, which lack protective IgA, had worsened blood sugar levels when fed a high fat diet
 

 

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On 8/20/2021 at 11:33 PM, Mike41 said:

Hi McCoy my 2 hour post prandials are around 95 after eating fruit, vegetables including potatoes.  Oatmeal with banana about the same. No added fats and no nuts, avocados etc.

Mike,  I too get back to baseline after 40 minutes of eating fruit. 2 hours is a standard benchmark but totally ignores the transients, peak values which may be very significant.

95 is a good baseline for a carbs eater, but I'd like at least a study with n=1000, I'm afraid n=1 is a tad too small of a sample!

All the above totally ignores personal propensities, which make the regimen tolerable and easy to adhere to the individual. What if I have a polymorphism which makes starches hard to digest to me (I have this suspicion). What if simple sugars tend to increase my glucose baseline, regardless of the fat content.

What if I have little or no insulin resistance guessable by the quick dissipation of glucose transients (regardless of my high fats consumption).

Literature has still very few examples. One CT means little. 5 CTs mean a little more.

10 CTs may start to clear up the subject. 30 CT can provide the basis for a scientific discussion, always keeping in mind that we cannot reason on the average response alone, there are the low percentiles, the high percentiles and the outliers.

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Dr. Klaper's clip.

I listened attentively to it, but the issue seems to be oversimplified.

First of all, keto diets are usually very rich in meats and saturated fats, with little or no protein restriction. That's not the classical keto diet, which entails protein restriction and severe carbohydrate restriction. The classic, real keto, indisputably sends a strong inhibitory signal to the mTORC pathway, depriving the path of the leucine and the glucose inputs. This may cause a decrease in weight and may cause an improvement or reversal in diabetes symptoms.

Hi protein keto, which is a variant of it, does continue to provide a significant leucine signal to the mTOR complex, plus the excess of amminoacids are converted to glucose by gluconeogenesis. So some glucose signal may be present too. mTOR is not so much inhibited.

Again, the usual keto is not a regime we would call healthy: lots of meats, cheese and saturated fats from many sources, in ponderous amounts. It may cause excessive blood lipids and inflammation.

The fact that glucose rises very much after ingestion of a carb meal while on keto is a known fact, which may not be due to fats-induced insulin resistance. It may be due to temporary inhibition of insulin release due to the very low ingestion of carbs. This phenomenon usually disappears after 2-3 days of carbs ingestion.

The evolution aspects and what our ancestors ate are not very relevant to longevity. We all know that our ancestors optimized their systems and diet toward survival and reproduction. It is a well-known fact that after reproduction age we are evolutionary expendable, which means that the optimization applicable to reproduction and survival is not applicable to healthspan and lifespan. 

In the end, what I criticize is the religious narrative about diet, be it from the paleo, the lowcarbers and the vegans. IF carbs are well tolerated, great , that's your good luck. IF carbs are not well tolerated, why should we endanger our health by keeping eating them, or go through restrictions (very low-fat) which do not agree with our own genetic makeup?

Last but not least, there is the middle way: eating modest amounts of carbs, the ones with less glicemic load, and eating healthy fats like EVOO. I don't know why we should be so attached to extremes. Keto is an extreme. VLF is another.

Edited by mccoy
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6 minutes ago, Mike41 said:

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

Quote

Funding
This work was funded by the Physicians Committee for Responsible Medicine.

This is the work of Neal Banard.  There are many doctors with extensive experience using ketogenic diets but Neal Banard is not one of them.

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I know Neal Barnard and we cannot say he's unbiased. For example, he has a strong bias toward fats (even the healthy ones) and dairy products (even the healthy ones). He wrote a whole book on the beta-casomorphins in cheese, contending that it contains opioids that cause addiction to it.

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8 hours ago, mccoy said:

Neal Barnard .. wrote a whole book on the beta-casomorphins in cheese, contending that it contains opioids that cause addiction to it. 

Yeah,  the book is titled:  "The Cheese Trap: How Breaking a Surprising Addiction Will Help You Lose Weight, Gain Energy, and Get Healthy".

Forbes article (2017):

Quote

...It turns out there’s a reason behind our [cheese] cravings. Cheese contains casein. It also contains casein fragments called casomorphins, a casein-derived morphine-like compound. Basically, dairy protein has opiate molecules built in. When consumed, these fragments attach to the same brain receptors that heroin and other narcotics attach to.

 'These opiates attach to the same brain receptors that heroin and morphine attach to. They are not strong enough to get you arrested, but they are just strong enough to keep you coming back for more, even while your thighs are expanding before your very eyes.' - Dr. Neal Barnard, author of The Cheese Trap

Some researchers believe this occurs as a way to ensure babies (humans, cows, etc.) continue to nurse during infancy, which helps the survival of the species. That helps explain why we look so happy when nursing and also why it feels so good to eat cheese. For perspective, a cup of milk contains 7.7 grams of protein, 80% of which is casein. When converted to cheddar, for example, the protein content multiplies 7-fold, to 56 grams. It’s the most concentrated form of casein in any food in the grocery store.

Basically, if milk is cocaine, then cheese is crack. [Lol !]

Our brain's ‘reward center’ releases dopamine when we eat salty foods like cheese in order to encourage us to eat more of it (many addictive drugs increase dopamine activity). Dopamine makes our bodies become attracted to whatever produced it, including cheese. Which is why so many people crave it, talk about it, and why even animal-loving vegetarians have a hard time giving it up.

Companies that sell cheese are well aware of these stats, and leverage our addiction to their benefit. Back in ‘00, at a presentation by Dairy Management Inc. (collects approximately $140 million each year from dairy companies to promote dairy products), they suggested that the key to increasing demand was to ‘trigger’ cheese cravings. 

The presenter broke cheese consumers into two categories: enhancers, those who sprinkle cheese on pasta, salad, etc. from time to time (not worth targeting), and cravers, people who LOVE cheese and will consume it whenever possible. This meant working with Fast Food companies to promote more cheese heavy products on their menus (Cheddar-Lovers sound familiar? Stuffed Crust pizza too!).  ETC.

 

Edited by Sibiriak
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On 8/23/2021 at 12:14 PM, mccoy said:

For example, he has a strong bias toward fats (even the healthy ones) and dairy products (even the healthy ones). He wrote a whole book on the beta-casomorphins in cheese, contending that it contains opioids that cause addiction to it.

Well, but perhaps Barnard is right and there are no "healthy fats" as far as processed or concentrated fats go (including any oils), and there is no "healthy dairy," other than breast milk during a limited time. BTW, the fat content of human milk is multiple times lower than that of cow milk (wrong assertion, corrected)

I used to love cheese, even while being a vegetarian, as well as olive oil. All I can say is that my blood panel is far better since I've practically eliminated cheese and dramatically limited EVOO.

One should also note that the adaptation to dairy is relatively rare in humans and it is unlikely to be optimized for longevity. It may simply be somewhat similar to the genetic adaptation of the Inuits to a high-fat diet.

Edited by Ron Put
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41 minutes ago, mccoy said:

I've nothing against Barnard, except the fact that he mistook diet for religion. Together with many others.

And how do you back that statement up with any evidence. The evidence for low fat whole plant based diets is not something crazy do you think? Did you See Dr. Freeman’s take on LFC DIETS ON the video Ron Putt just posted? I GUESS HES A RELIGIOUS FANATIC TOO!

 

Edited by Mike41
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Haha, I just thought of it on my walk and came back to correct :D
Of course, you are right. I am reading and listening to stuff on milk allergies and lactose intolerance today and my mind is on proteins... Cow milk contains 2-4 times as much protein as human milk, with much greater quantities of leucine and it greatly increases serum levels of insulin and IGF-1. Cow milk also has a much higher proportion of caseins than human milk, too.

As to fat, human milk can actually be a bit higher in fat content. But cow milk has a significantly higher proportion of saturated fats, and human milk is much higher in unsaturated fats, including  Omega-3s.

Edited by Ron Put
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1 hour ago, Ron Put said:

But cow milk has a significantly higher proportion of saturated fats, and human milk is much higher in unsaturated fats, including  Omega-3s.

Human milk fatty acid composition has been shown to be heavily influenced by dietary fatty acids. De novo lipogenesis primarily produces saturated fatty acids but for most people the contribution from DNL is a fraction of what comes from diet. 

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13 hours ago, Ron Put said:

As to fat, human milk can actually be a bit higher in fat content. But cow milk has a significantly higher proportion of saturated fats, and human milk is much higher in unsaturated fats, including  Omega-3s.

There are always low-fat and non-fat brands of cow milk in commerce. 

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