Regaining weight post diet/exercise due to lowered metabolism by increased PUFA in cardiolipin

[haidut]

This is by far the most significant study I have seen come out in the last 2-3 years, simply because of the impact it has on virtually every person out there who has tried to lose excess weight (and who hasn't?). Virtually every person considering (or having done) dieting/exercise to lose excess weight dreads the infamous "rebound". You see, losing weight is not that hard for most people, even the weak-willed couch potatoes. It is keeping it off after losing it that is the hard part. Years ago, I posted about a study on the contestants in the show the Biggest Loser.

"Biggest Loser" Contestants Regained Weight. Peat Perspective

As I explained in that post, not only had all of them regained the lost weight within 6 months after leaving the show, but many of them found out they surpassed their original weight even on a lower-calorie diets. How could this be!?? Well, the study on the Biggest Loser found out that the resting metabolic rate of the contestants had plummeted as a result of the drastic weight loss they had endured, so when they stopped the grueling regimen those poor souls had the metabolic rate of turtles (famously slow metabolizers). Worse, in the process of losing that excess weight, the contestants lost a majority of their lean muscle mass and by the time they were done with the show they all had some degree of the so-called "sarcopenic obesity" (colloquially known as "skinny-fat"), which even doctors dread as they know this condition is a very good predictor of future mortality and morbidity and puts people with that condition at a higher risk than even the morbidly obese people that those "losers" used to be. Lean muscle mass is one of the primary determining factors of the resting metabolic rate (RMR) and losing it through severe dieting and/or exhaustive exercise is one of the worst outcomes one can "achieve" with such regimens.

Now, the study below demonstrates that the dastardly PUFA plays a central role in this fiasco. The study confirmed again that weight loss reduced RMR, and found that the mechanism behind this reduction in RMR is the increased proportion of PUFA-containing phospholipids in cardiolipin (the crucial mitochondrial enzyme, largely controlling the speed of OXPHOS). Specifically, the study found that weight loss through dieting/exercise increased the content of the omega-6 linoleic acid phospholipid species composing cardiolipin. Dr. Peat mentioned in several of his interviews that the lipid composition of cardiolipin changes over the lifespan of a human (and most mammals), being composed of mostly saturated fats in childhood and progressively switching to PUFA species in adulthood and old age (the same process is seen in most chronic diseases too). Conversely, several studies have shown that feeding old animals lipids completely devoid of PUFA can change the cardiolipin composition back to a more PUFA-deficient state and restore the metabolic rate of even very old animals back to youthful levels. The human equivalent dose (HED) of that PUFA-deficient lipid feeding study was ~200mg/kg, so for most humans a daily dose of 15g-20g of coconut or moringa oils (both have very low PUFA content), or a completely hydrogenated oil (as the study used, but more difficult to obtain) may be able to prevent/reverse the decline in metabolic rate seen after dieting/exercising people and/or even old age.

https://academic.oup.com/lifemeta/article/doi/10.1093/lifemeta/load014/7103241?login=false

Increasing skeletal muscle mitochondrial efficiency after weight loss as a novel mechanism for lower energy expenditure

Weight regain is a common problem for weight loss individuals. A number of studies have shown that weight loss in overweight people results in a reduction in whole-body energy expenditure.

medicalxpress.com

Enhancing Muscle Mitochondrial Efficiency After Weight Loss

"...Regaining weight is a prevalent issue among individuals who have lost weight. Several research studies indicate that overweight individuals experience a decrease in overall energy expenditure after shedding pounds. This decline in energy expenditure disproportionately affects different tissues, resulting in an energetic mismatch. This imbalance is primarily due to a reduction in lean tissue, thereby increasing the likelihood of regaining weight. Despite identifying this phenomenon, the precise mechanisms of how weight loss affects skeletal muscle mitochondrial respiration remain unknown, and concrete evidence is yet to be established. In April 2023, Life Metabolism featured a study by Professor Katsuhiko Funai at the University of Utah titled "Weight loss elevates skeletal muscle mitochondrial energy efficiency in obese mice." The research team discovered that obese mice undergoing weight loss experienced an improvement in the efficiency of skeletal muscle mitochondrial oxidative phosphorylation, leading to decreased energy expenditure throughout the body. This reduction in energy expenditure may contribute to weight regain following weight loss."

"...To investigate the effects of weight loss on mitochondrial energy metabolism, researchers conducted a study using obese mice treated with dietary interventions to induce weight loss. High-resolution respirometry and fluorometry measurements were used to assess changes in mitochondrial energy metabolism, while mitochondrial proteomes and lipidomes were analyzed to examine any related changes. The results showed that while there was no significant change in mitochondrial proteomes or respiratory chain supercomplex formation, weight loss did lead to an increase in oxidative phosphorylation efficiency (as seen in Figure 1). Additionally, the researchers found that weight loss accelerated the remodeling of mitochondrial cardiolipin (CL) acyl-chains, resulting in an increase in the content of tetralinoleoyl CL (TLCL), a lipid species believed to be critical for respiratory enzymes. Knocking down the CL acyltransferase tafazzin was shown to reduce TLCL levels and skeletal muscle oxidative phosphorylation levels, allowing mice to avoid diet-induced weight gain (also shown in Figure 1). Taken together, these findings suggest that weight loss can increase skeletal muscle mitochondrial energy production efficiency, leading to a reduction in overall energy expenditure in the body."

 

[Hans]

This is by far the most significant study I have seen come out in the last 2-3 years, simply because of the impact it has on virtually every person out there who has tried to lose excess weight (and who hasn't?). Virtually every person considering (or having done) dieting/exercise to lose excess weight dreads the infamous "rebound". You see, losing weight is not that hard for most people, even the weak-willed couch potatoes. It is keeping it off after losing it that is the hard part. Years ago, I posted about a study on the contestants in the show the Biggest Loser.

"Biggest Loser" Contestants Regained Weight. Peat Perspective

As I explained in that post, not only had all of them regained the lost weight within 6 months after leaving the show, but many of them found out they surpassed their original weight even on a lower-calorie diets. How could this be!?? Well, the study on the Biggest Loser found out that the resting metabolic rate of the contestants had plummeted as a result of the drastic weight loss they had endured, so when they stopped the grueling regimen those poor souls had the metabolic rate of turtles (famously slow metabolizers). Worse, in the process of losing that excess weight, the contestants lost a majority of their lean muscle mass and by the time they were done with the show they all had some degree of the so-called "sarcopenic obesity" (colloquially known as "skinny-fat"), which even doctors dread as they know this condition is a very good predictor of future mortality and morbidity and puts people with that condition at a higher risk than even the morbidly obese people that those "losers" used to be. Lean muscle mass is one of the primary determining factors of the resting metabolic rate (RMR) and losing it through severe dieting and/or exhaustive exercise is one of the worst outcomes one can "achieve" with such regimens.

Now, the study below demonstrates that the dastardly PUFA plays a central role in this fiasco. The study confirmed again that weight loss reduced RMR, and found that the mechanism behind this reduction in RMR is the increased proportion of PUFA-containing phospholipids in cardiolipin (the crucial mitochondrial enzyme, largely controlling the speed of OXPHOS). Specifically, the study found that weight loss through dieting/exercise increased the content of the omega-6 linoleic acid phospholipid species composing cardiolipin. Dr. Peat mentioned in several of his interviews that the lipid composition of cardiolipin changes over the lifespan of a human (and most mammals), being composed of mostly saturated fats in childhood and progressively switching to PUFA species in adulthood and old age (the same process is seen in most chronic diseases too). Conversely, several studies have shown that feeding old animals lipids completely devoid of PUFA can change the cardiolipin composition back to a more PUFA-deficient state and restore the metabolic rate of even very old animals back to youthful levels. The human equivalent dose (HED) of that PUFA-deficient lipid feeding study was ~200mg/kg, so for most humans a daily dose of 15g-20g of coconut or moringa oils (both have very low PUFA content), or a completely hydrogenated oil (as the study used, but more difficult to obtain) may be able to prevent/reverse the decline in metabolic rate seen after dieting/exercising people and/or even old age.

https://academic.oup.com/lifemeta/article/doi/10.1093/lifemeta/load014/7103241?login=false

Increasing skeletal muscle mitochondrial efficiency after weight loss as a novel mechanism for lower energy expenditure

Weight regain is a common problem for weight loss individuals. A number of studies have shown that weight loss in overweight people results in a reduction in whole-body energy expenditure.

medicalxpress.com

Enhancing Muscle Mitochondrial Efficiency After Weight Loss

"...Regaining weight is a prevalent issue among individuals who have lost weight. Several research studies indicate that overweight individuals experience a decrease in overall energy expenditure after shedding pounds. This decline in energy expenditure disproportionately affects different tissues, resulting in an energetic mismatch. This imbalance is primarily due to a reduction in lean tissue, thereby increasing the likelihood of regaining weight. Despite identifying this phenomenon, the precise mechanisms of how weight loss affects skeletal muscle mitochondrial respiration remain unknown, and concrete evidence is yet to be established. In April 2023, Life Metabolism featured a study by Professor Katsuhiko Funai at the University of Utah titled "Weight loss elevates skeletal muscle mitochondrial energy efficiency in obese mice." The research team discovered that obese mice undergoing weight loss experienced an improvement in the efficiency of skeletal muscle mitochondrial oxidative phosphorylation, leading to decreased energy expenditure throughout the body. This reduction in energy expenditure may contribute to weight regain following weight loss."

"...To investigate the effects of weight loss on mitochondrial energy metabolism, researchers conducted a study using obese mice treated with dietary interventions to induce weight loss. High-resolution respirometry and fluorometry measurements were used to assess changes in mitochondrial energy metabolism, while mitochondrial proteomes and lipidomes were analyzed to examine any related changes. The results showed that while there was no significant change in mitochondrial proteomes or respiratory chain supercomplex formation, weight loss did lead to an increase in oxidative phosphorylation efficiency (as seen in Figure 1). Additionally, the researchers found that weight loss accelerated the remodeling of mitochondrial cardiolipin (CL) acyl-chains, resulting in an increase in the content of tetralinoleoyl CL (TLCL), a lipid species believed to be critical for respiratory enzymes. Knocking down the CL acyltransferase tafazzin was shown to reduce TLCL levels and skeletal muscle oxidative phosphorylation levels, allowing mice to avoid diet-induced weight gain (also shown in Figure 1). Taken together, these findings suggest that weight loss can increase skeletal muscle mitochondrial energy production efficiency, leading to a reduction in overall energy expenditure in the body."

I doubt this study is of any use though...

They said: "Last but not least, we did not test whether TAZ knockdown would make mice resistant to weight loss-induced reduction in energy expenditure and an increase in muscle OXPHOS efficiency"

In the abstract they said tafazzin knockdown allowed mice to avoid diet-induced weight gain, but later on they say that they didn't test it.

Also, after they made the animals fat on an obesogenic 40% fat diet, they switch half of them back to chow diet. The cardiolipin will of course remodel once the fat content changes/reduces. They didn't lose weight below baseline. They were just basically given the same amount of food as the control group. They were taken out of a surplus. Hence...fat loss.

With the TAZ knockdown, all cardiolipin decreased and ATP dropped. But O2 consumption did not increase. That means they did not get a boost in metabolism. DNP or caffeine or aspirin increases O2 consumption.

The reason people rebound is because they can't stick to the diet anymore and start overconsuming calories. The drop in metabolism from fat loss is because they lost weight. Less weight = less metabolically active tissue and less weight to carry around = "slower" metabolic rate.

This is why there was zero fat gain in the concentration camps. Zero "rebound" if calories don't increase. Rebound is only due to an overconsumption of food.

 

[Hans]

Another important thing to note is that they didn't put the mice in a deficit for fat loss. They only put them back on the control diet, so they regained the cardiolipin that the control group had. Thus, the control group also had high linoleic acid cardiolipin, but they didn't become obese. It would have been more interesting if they just cut the calories of the obesogenic diet, instead of completely changing their diets.

There was another interesting study where they gave old animals 100% hydrogenated peanut oil, and as a result, the linoleic acid in their cardiolipin went up. As we know, linoleic in cardiolipin is what healthy animals and humans have; sick people and animals have longer chain, more unsaturated fats, like arachidonic acid, in their cardiolipin.

Lastly, more ATP production is a good thing. Dysfunctional mitochondria don't produce energy. Restoring the obese mice's cardiolipin back to the more "healthy" control group's cardiolipin, boosted their ATP. Obese people struggle with low energy. Generally, losing weight boosts energy. If the deficit, however, is too big and the exercise too much, ofc that is unhealthy and drains too much energy.
Type 1 diabetics, with zero insulin, also don't gain fat. But they still die young if untreated.

 

[haidut]

..

 

[haidut]

Thus, the control group also had high linoleic acid cardiolipin, but they didn't become obese.

The study did not compare cardiolipin composition of the LN group so we don't know how much PUFA their cardiolipin had. That being said, when you eat more fat, with proportionally more PUFA in it, the expected effects are to have more PUFA stored into adipocytes. Then, when commencing dieting/fasting, lipolysis preferentially releases PUFA from adipocytes and this exposes cells in the body to a fat supply that is almost 100% PUFA. That is the really the gist of the study (at least to me) - i.e. dieting increases PUFA-ication of cardiolipin, which lowers energy expenditure, often leading to weight regain. In other words two lean people with identical weight, but one naturally lean and the other one lean due to fasting/exercise won't end up with the same weight when eating the same daily caloric intake over time. The unnaturally lean person will gain more weight on the same caloric intake due to lower metabolic rate and increased cardiolipin unsaturation. All of that has been mentioned by Ray and, to me at least, this study is a corroboration of his recommendations against chronic fasting.

 

[haidut]

..

 

[haidut]

The drop in metabolism from fat loss is because they lost weight. Less weight = less metabolically active tissue and less weight to carry around = "slower" metabolic rate.

Not sure about that. The drop in metabolism from dieting/exercise is mostly linked to the loss of lean muscle mass, which is more metabolically active and responsible for most of the fat burning one does (at rest). The study itself hints to the lean mass loss and its change of metabolic efficiency, but other studies (human) have had similar findings. The experimental data shows dieting/exercise induced caloric deficit results in a 1:1-1:2 ratio of muscle:fat loss, and even the 1:1 ratio loss is pretty bad outcome.

Intermittent Fasting and Potential Loss of Muscle Mass

Lean body mass as well as fat stores are lost, according to a new study.

www.psychologytoday.com

If you look at those studies on the Biggest Loser contestants - most of them regained the weight on even less calories then they were eating before. Yes, they did not stick to the X calories they ate during the study but many/most did not go back to the Y calories (Y>>X) they ate before the show and still regained (and even exceeded) their original weight. Some of them got diagnosed with sarcopenic obesity, which they did not have before and this proves they lost more muscle than fat.
As far as zero rebound if calories don't increase - sure, but that is not the argument here. Using X and Y as above example of Biggest Loser, assuming Y = 4*X (just for argument sake), the people that finished the Biggest Loser show while eating X calories daily then regained (and even exceeded) their original pre-show weight on 2*X calories, not 4*X (4*X=Y, the original caloric intake before the show). That speaks of severely reduced metabolic rate, which is what both the Biggest Loser post/study and this study demonstrated. Most of that metabolic rate decline is from muscle loss.
Concentration camp survivors have been shown to have strikingly reduced metabolic rates and most got very fat and ill when they went on a normal calorie diet. Ray has some quotes and studies about their prolactin being so high from the stress in the camp that they were lactating at the time they got liberated. In such a metabolic state, I would not be surprised if even 500 calories daily get those people fat.
They did test tafazzin knockdown for avoiding weight gain and it worked. Look at Figure 5.
"...We investigated whether TLCL influences OXPHOS efficiency to alter the propensity for weight gain. For these experiments, we utilized mice with doxycycline-induced whole-body knockdown of TAZ (TAZKD mice) compared to doxycycline-fed WT littermates (Fig. 5a). Previous studies have shown that TAZKD mice exhibit greater energy expenditure and are protected from diet-induced obesity [34, 36]. Our observations recapitulated these findings (Fig. 5b and c)."

 

[haidut]

Lastly, more ATP production is a good thing. Dysfunctional mitochondria don't produce energy. Restoring the obese mice's cardiolipin back to the more "healthy" control group's cardiolipin, boosted their ATP.

More ATP is not always good. Cancer cells produce a ton of ATP, through through glycolysis instead of OXPHOS. ATP also has a negative feedback cycle with pyruvate dehydrogenase, so maximizing ATP production is not desirable. The best health outcomes are seen in moderately uncoupled states and, as you know, that is what DNP does and this is why it is being proposed for treatment of diabetes, CVD, and even cancer.

 

[Mr Joe]

More ATP is not always good. Cancer cells produce a ton of ATP, through through glycolysis instead of OXPHOS. ATP also has a negative feedback cycle with pyruvate dehydrogenase, so maximizing ATP production is not desirable. The best health outcomes are seen in moderately uncoupled states and, as you know, that is what DNP does and this is why it is being proposed for treatment of diabetes, CVD, and even cancer.

The negative feedback is only for ATP created through glycolysis or doest creating ATP with OXPHOS has also a negative feed back (Or maybe bad feedback is inhibited/protected by high CO2 production in Oxphos?) ?

 

[haidut]

As we know, linoleic in cardiolipin is what healthy animals and humans have; sick people and animals have longer chain, more unsaturated fats, like arachidonic acid, in their cardiolipin.

Agreed with the second part, though not the first. Late teen and adult humans do have more linoleic acid in their cardiolipin but that does not make it healthy. The study above demonstrated that energy expenditure is higher when there is less linoleic acid in the cardiolipin. Also, human mortality is lowest in the age period 10-12, when metabolic rate peaks, and cardiolipin composition is mostly saturated phospholipids until that age. Then, it starts changing towards more omega-6, as seen in most adults, and in extreme age/diseases the omega-3 species, as you said predominate. Btw, those studies on cardiolipin composition and modification of its composition by dietary fats are linked in my post, before the study quotes start.
Anyways, medicine calls saturated-phospholipid-dominant cardiolipin "immature" but that is simply an observational statement as such a state is seen mostly in children up to the age of about 12. It does not mean that "mature" cardiolipin (high in linoleic acid) is a good thing. I guess it is an intermediary state of unsaturation until old age or disease kick in and then omega-3 species inside cardiolipin take over. Lowering ATP synthesis in favor of more heat production, by changing cardiolipin structure, has long been known to be a viable pathway for curing obesity and diabetes, and without side effects such as loss of lean muscle mass that dieting and/or exhaustive exercise induce. If anything, the study above and the second one below show that increased metabolic efficiency is a bad thing and leads to obesity/diabetes/etc. PUFA increases the metabolic efficiency, so its dominance in adult cardiolipin probably explains to a great degree the steady weight gain post the age of about 25.

Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer

Cardiolipins (CLs) are specific phospholipids of the mitochondria composing about 20% of the inner mitochondria membrane (IMM) phospholipid mass. Dysregulation of CL metabolism has been observed in several types of cancer. In most cases, the evidence ...

www.ncbi.nlm.nih.gov

"...Finally, CL synthase 1 (CRLS1) catalyzes the formation of immature CL by using CDP-DG and PG [17]. Immature CLs are characterized by saturated acyl chains of variable length and asymmetry around the glycerol head group [18,19]."

https://www.science.org/doi/10.1126/sciadv.abd6322

"...Unbalanced energy partitioning participates in the rise of obesity, a major public health concern in many countries. Increasing basal energy expenditure has been proposed as a strategy to fight obesity yet raises efficiency and safety concerns. Here, we show that mice deficient for a muscle-specific enzyme of very-long-chain fatty acid synthesis display increased basal energy expenditure and protection against high-fat diet–induced obesity. Mechanistically, muscle-specific modulation of the very-long-chain fatty acid pathway was associated with a reduced content of the inner mitochondrial membrane phospholipid cardiolipin and a blunted coupling efficiency between the respiratory chain and adenosine 5′-triphosphate (ATP) synthase, which was restored by cardiolipin enrichment. Our study reveals that selective increase of lipid oxidative capacities in skeletal muscle, through the cardiolipin-dependent lowering of mitochondrial ATP production, provides an effective option against obesity at the whole-body level."

Finally, while the study in OP did not look into this, other studies demonstrated directly that inhibition (or lack) of tafazzin directly changes cardiolipin composition back to a more saturated phenotype, and that leads to less ATP, more heat, and higher energy expenditure - i.e the 12-year old child phenotype. PUFA does the opposite.

What Links Neutropenia to Immature Cardiolipin in Patients with Barth Syndrome (tafazzin-deficiency)?

Barth syndrome is an inherited X-linked disorder characterized by cardiomyopathy, skeletal muscle myopathy, and neutropenia. The syndrome arises because of inhe

ashpublications.org

"...Tafazzin is an enzyme that processes the final step of cardiolipin maturation, replacing saturated with unsaturated acyl chains. Cardiolipin is a 4-tailed phospholipid that is almost-exclusively found in the inner membrane of the mitochondria. The lack of tafazzin activity results in a cardiolipin pool that contains more highly saturated lipid tails..."

 

[haidut]

The negative feedback is only for ATP created through glycolysis or doest creating ATP with OXPHOS has also a negative feed back (Or maybe bad feedback is inhibited/protected by high CO2 production in Oxphos?) ?

Any ATP excess will limit PDH activity. This is one reason PDH is low in cancer cells - i.e. they have plenty of (glycolysis-derived) ATP to limit PDH. However, supplying some precursors such as succinic acid, as well as cofactors needed for mitochondrial ATP synthesis has been shown to restrain the excessive ATP production from glycolysis and this reduce the lactate generation of cancer cells as well as delay/ameliorate the cachexia this abnormal ATP generation (and other factors) cause in cancer patients. The Cardenosine thread has a study showing significant tumor reduction when ATP or succinic acid are injected into tumor-bearing animals.

 

[Highserotonin90]

In summary ... can we take extra virgin olive oil which is rich in linoleic acid or is it counterproductive? beyond the PUFA content.

 

[haidut]

In summary ... can we take extra virgin olive oil which is rich in linoleic acid or is it counterproductive? beyond the PUFA content.

Olive oil is fine in moderation. I would not call it "rich' in linoleic acid, it has about 8% on average. Just don't overconsume it (2-3 tablespoons daily is probably OK), relative to saturated fat. The bigger worry is all the other PUFA-laden oils we consume daily from commercial foods. If that PUFA can be eliminated/reduced it would have a much bigger impact than consuming or not consuming olive oil.

 

[cremes]

The human equivalent dose (HED) of that PUFA-deficient lipid feeding study was ~200mg/kg, so for most humans a daily dose of 15g-20g of coconut or moringa oils (both have very low PUFA content), or a completely hydrogenated oil (as the study used, but more difficult to obtain) may be able to prevent/reverse the decline in metabolic rate seen after dieting/exercising people and/or even old age.

I follow along here at the Peat forum and also keep track of Brad Marshal's videos and posts. There's a nice coincidence here where his latest video speaks directly to the issue of how to resaturate our tissues with coconut oil. In the video he says that the medium chain fatty acids, specifically C8 and C10, are burned for energy relatively quickly. The long chain fats, C16 and C18, are desaturated and stored as oleic in our bodies. Lastly, the "intermediate" length fatty acids, C12 and C14, are apparently stored. Not only are they stored, but in mouse studies they push out PUFA and MUFA and can resaturate our tissues.


View: https://www.youtube.com/watch?v=bJUBPlGXjtk&t=3s


I started a simpler mono diet a few weeks ago to try and get my thyroid revved up again without taking any directly. OJ, fat-free milk, a raw carrot, fresh oranges or pineapple, baked potatoes that are then peeled and fried in CO, and hot sauce for flavor. I just measured this morning and confirmed that I am consuming about 30 grams of coconut oil a day along with around 1kg of fried potato. Cronometer puts the oil at around 330 calories and the potatoes at another 1100 calories. I need the OJ, carrot, and fruit to bump my numbers and even then the calories are too low at about 2k per day. I'm 6', 210 lbs, male, 50, so my BMR is about 2600/day. I'm not hungry though.

I am also taking 1.5 grams (divided) of crushed black cumin. I noticed an early heat effect but it has diminished. I also take ~250mg of niacinamide (divided) per day. Waking temps are 97.5 and daytime temps hover around 96.8 all day.

So far over the last 2 weeks my weight has moved up about 3 pounds. I'll keep this up for another month and see where I end up. If I push 220, I'm gonna be pissed. :)

 

[haidut]

Lastly, the "intermediate" length fatty acids, C12 and C14, are apparently stored. Not only are they stored, but in mouse studies they push out PUFA and MUFA and can resaturate our tissues.

Very interesting, thanks. Can you please share the animals studies with those fatty acids?

 

[cremes]

Very interesting, thanks. Can you please share the animals studies with those fatty acids?

Here's the paper that Brad posted in one of his reddit threads.

https://sci.bban.top/pdf/10.1016/s0021-9258%252818%252976693-3.pdf

I hadn't read it until now. This paper is almost 100 years old and still very relevant.

There's another paper that looks at the fat composition of swine fed coconut oil but I don't have access to it beyond the abstract.

https://academic.oup.com/jas/article-abstract/33/2/370/4697577

 

[MikeyFitz]

I follow along here at the Peat forum and also keep track of Brad Marshal's videos and posts. There's a nice coincidence here where his latest video speaks directly to the issue of how to resaturate our tissues with coconut oil. In the video he says that the medium chain fatty acids, specifically C8 and C10, are burned for energy relatively quickly. The long chain fats, C16 and C18, are desaturated and stored as oleic in our bodies. Lastly, the "intermediate" length fatty acids, C12 and C14, are apparently stored. Not only are they stored, but in mouse studies they push out PUFA and MUFA and can resaturate our tissues.


View: https://www.youtube.com/watch?v=bJUBPlGXjtk&t=3s


I started a simpler mono diet a few weeks ago to try and get my thyroid revved up again without taking any directly. OJ, fat-free milk, a raw carrot, fresh oranges or pineapple, baked potatoes that are then peeled and fried in CO, and hot sauce for flavor. I just measured this morning and confirmed that I am consuming about 30 grams of coconut oil a day along with around 1kg of fried potato. Cronometer puts the oil at around 330 calories and the potatoes at another 1100 calories. I need the OJ, carrot, and fruit to bump my numbers and even then the calories are too low at about 2k per day. I'm 6', 210 lbs, male, 50, so my BMR is about 2600/day. I'm not hungry though.

I am also taking 1.5 grams (divided) of crushed black cumin. I noticed an early heat effect but it has diminished. I also take ~250mg of niacinamide (divided) per day. Waking temps are 97.5 and daytime temps hover around 96.8 all day.

So far over the last 2 weeks my weight has moved up about 3 pounds. I'll keep this up for another month and see where I end up. If I push 220, I'm gonna be pissed. :)

Do you think your coconut oil calories could be too high?

Yes, it's the best form of fat, but it's still fat.

You and I are almost exactly the same height and weight but I am a little older at 59 yrs old.

As soon as I lowered my fat calories to about 10% and made up the difference with ripe fruit and simple sugars, my BMR went up and I began losing fat very quickly.

I eat very ripe fruit all day covered in real sugar or organic maple syrup.

I also eat organic Greek non-fat yogurt as my protein covered in sugar or organic maple syrup. One 32oz container has 80g of protein.

I add 5 grams of glycine total for the day, spread out over all of my meals.

For dinner post-workout I usually have very well-cooked Sushi rice, sauteed chicken breast with a small amount of chicken liver, added glycine, and orange marmalade sauce.

In the morning I take the following supplements:

1 packet of BC aspirin powder (dissolved in OJ).

10 mg of Methylene Blue in a gelatin capsule and take it with the aspirin/OJ combo.

5 mg of DHEA and a large dose of Pregnenolone 150 mg.

A gelatin capsule with 10 drops of Energin along with an extra 500 mg capsule of Thorne Niacinamide.

A gelatin capsule with 20 drops of Pyrucet.

1 grain of Armour Thyroid.


At night I take the following:

1 grain Armour Thyroid

5mg DHEA with 40mg Pregnenolone and 500mg Thorne Niacinamide

A very high sugar snack or drink

 

[Hans]

The reason why I'm writing on this is because people are looking for excuses not to implement the right dietary guidelines and habits to lose weight. Thus they never get to their goal. They are always looking for "tricks" like this to lose weight. Tricks like using aspirin, caffeine, restricting protein, restricting exercise, supplementing coconut oil, etc.
They just end up spinning their wheels.
There are very few people that reached their goal weight on this forum. Most people blow up because they overconsume calories. Regardless of how hard they try to restrict PUFA.
People who reach their goal weight either implement the right basic strategies or accidentally discover a diet that blunts their appetite and/or dramatically increase their energy.

The study did not compare cardiolipin composition of the LN group so we don't know how much PUFA their cardiolipin had.

Yes exactly, so it's wrong of the researchers to assume that the linoleic acid in the cardiolipin is what's causing the rebound, since it could have been the same as the control group.

That being said, when you eat more fat, with proportionally more PUFA in it, the expected effects are to have more PUFA stored into adipocytes. Then, when commencing dieting/fasting, lipolysis preferentially releases PUFA from adipocytes and this exposes cells in the body to a fat supply that is almost 100% PUFA.

The studies I've seen show that cardiolipin reflects the diet. People that are obese are more unhealthy than people who aren't. Yes, some obese individuals are healthier than other obese peeps, but lean individuals are almost always healthier.

That is the really the gist of the study (at least to me) - i.e. dieting increases PUFA-ication of cardiolipin, which lowers energy expenditure, often leading to weight regain.

I don't think we can deduce that from the study since they did not look at the cardiolipin of the control group. If an obese individual was to go live on an island where everyone is lean and healthy and eat their diet, that person will soon lose all the weight and look like the people there.

In other words two lean people with identical weight, but one naturally lean and the other one lean due to fasting/exercise won't end up with the same weight when eating the same daily caloric intake over time. The unnaturally lean person will gain more weight on the same caloric intake due to lower metabolic rate and increased cardiolipin unsaturation.

I can't agree with this. What I've observed is that it comes down to how energized a diet makes you feel. If someone is in a deficit and they are super tired, they will not move and thus very little weight loss will occur.
If that same person creates a deficit with a diet that makes them feel energized, they will move more and not be tired.
This has happened many times with me. I struggle to lose weight on 2000 calories, then I add more carbs and eat 2500 calories and suddenly I lean down... Is it because I eat more? No, my activity level goes up significantly because I feel a lot better.

Not sure about that. The drop in metabolism from dieting/exercise is mostly linked to the loss of lean muscle mass, which is more metabolically active and responsible for most of the fat burning one does (at rest). The study itself hints to the lean mass loss and its change of metabolic efficiency, but other studies (human) have had similar findings. The experimental data shows dieting/exercise induced caloric deficit results in a 1:1-1:2 ratio of muscle:fat loss, and even the 1:1 ratio loss is pretty bad outcome.

We're basically saying the same thing. Deficits waste muscle unless that person also lifts weights and eats enough protein. Else they will just become a smaller version of what they already look like (smaller skinny fat version).

If you look at those studies on the Biggest Loser contestants - most of them regained the weight on even less calories then they were eating before. Yes, they did not stick to the X calories they ate during the study but many/most did not go back to the Y calories (Y>>X) they ate before the show and still regained (and even exceeded) their original weight.

Yes because their activity level tanks. It's a compensation mechanism. Either appetite goes up, activity goes down or both. Biggest loser follow the worse diet and training protocols so it's definitely not a good example.

Concentration camp survivors have been shown to have strikingly reduced metabolic rates and most got very fat and ill when they went on a normal calorie diet. Ray has some quotes and studies about their prolactin being so high from the stress in the camp that they were lactating at the time they got liberated. In such a metabolic state, I would not be surprised if even 500 calories daily get those people fat.

There are many things at play with their rebound. Prolactin causes weight gain due to enhances appetite. They likely ate in a massive surplus, didn't move at all (traumatized and fatigued) and had severe nutritional deficiencies.

More ATP is not always good. Cancer cells produce a ton of ATP, through through glycolysis instead of OXPHOS. ATP also has a negative feedback cycle with pyruvate dehydrogenase, so maximizing ATP production is not desirable. The best health outcomes are seen in moderately uncoupled states and, as you know, that is what DNP does and this is why it is being proposed for treatment of diabetes, CVD, and even cancer.

Yes I understand that, but this study didn't prove that this ATP boost was leading to problems. It was likely a normalization of ATP production.
When someone uses DNP, oxygen consumption skyrockets. In this study, O2 consumption remained the same. How could they be burning the same amount of calories (either to ATP or heat), but magically get leaner? If their metabolisms got really fast due to low PUFA in cardiolipin, O2 consumption would have gone up.

The study above demonstrated that energy expenditure is higher when there is less linoleic acid in the cardiolipin.

How did they prove that? O2 remained the same as I mentioned above.

 

[Hans]

Also, human mortality is lowest in the age period 10-12, when metabolic rate peaks, and cardiolipin composition is mostly saturated phospholipids until that age. Then, it starts changing towards more omega-6, as seen in most adults, and in extreme age/diseases the omega-3 species, as you said predominate.

I have never found evidence to support that claim. From the studies I've found, like this one (children under 18 with heart disease), had preserved tetralinoleoyl CL species compared to their health counterparts.
Thyroid hormone has also been shown to enhance cardiolipin production and incorporate unsaturated fat into it:
"Treatment with thyroxine resulted in a 1.8-fold increase (P<0.025) in [1-(14)C]linoleate and a 1.7-fold increase (P<0.025) in [1-(14)C]oleate incorporated into cardiolipin in perfused hearts, compared with controls. The mechanism for the elevation in incorporation of unsaturated fatty acids into cardiolipin was a 1. 6-fold (P<0.025) increase in mitochondrial monolysocardiolipin acyltransferase activity." (R)

PUFA increases the metabolic efficiency, so its dominance in adult cardiolipin probably explains to a great degree the steady weight gain post the age of about 25.

Weight gain after 25 is due to inactivity and eating more. Who after 25 are as active as they used to be before 25? Or eat the same diet?
PUFA (e.g. arachidonic acid) in cardiolipin makes it more fluid, which makes the ETC leaky. It makes it less effective, not more effective. Linoleic acid rich cardiolipin makes the mitochondria more effective aka restores proper mitochondrial function.
I'm not saying to eat a lot of linoleic acid. As I pointed out earlier, giving animals 100% hydrogenated peanut oil restored the linoleic content in their cardiolipin.

If anything, their study shows that not having cardiolipin protects against obesity.

I understand that uncoupling is key to fat loss, but nothing that we do is going to give us any phenomenal results. DNP works because it enhances energy out. Nothing else comes close.

 

[cremes]

Do you think your coconut oil calories could be too high?

Yes, it's the best form of fat, but it's still fat.

You and I are almost exactly the same height and weight but I am a little older at 59 yrs old.

As soon as I lowered my fat calories to about 10% and made up the difference with ripe fruit and simple sugars, my BMR went up and I began losing fat very quickly.

It's possible that my fat calories are too high. I punched everything into cronometer to get a reading and this is what it shows.

I can try upping the sugar or honey, but I'm just not hungry. Yet my weight isn't moving.

A year ago I just would have done a 3-day fast but that likely contributed to my broken metabolism. I'm just going to keep on trucking here... I'll keep calories as high as I can for as long as I can and see where the chips fall. One of the benefits of being older is stubborness; I have that in spades now.