Does being in ketosis automatically translate to fat loss? NO - Dr. Peter Attia

(Bunny) #1

How to make a fat cell less not thin: the lessons of fat flux One of the questions I (Dr. Peter Attia) most often receive: Does being in ketosis automatically translate to fat loss?

For those too busy to read ahead, let me give you the punch line: No. For those who want to understand why, keep reading (hopefully this is still everyone). This topic is — surprise, surprise — very nuanced, and almost always bastardized when oversimplified, which I’m about to do, though hopefully less than most. Without oversimplifying, though, this will turn into a textbook of 1,000 pages. …More

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Notable Quotations:

”…They are not giving up fat from their fat cells because they are eating less. They are eating less because they are giving up fat from their fat cells. Big difference. (*) The especially astute reader will note that this is the first time I have made reference to this point. I have been heavily influenced recently by the work of Mark Friedman, and a discussion of this point is worth an entire post, which I promise to deliver at some point in the future. If you can’t wait, which I can understand, I highly encourage you to start scouring the literature for Mark’s work. It’s simply remarkable. …”

”…Nutritional ketosis is one eating strategy to facilitate negative fat flux, and it works very well if done correctly. …”

A Calorie is Not A Calorie - A Discussion of Thermodynamics
Feeling "high" with high readings?
(Bunny) #2

Research citations: Mark Friedman

  1. When do we eat? Ingestive behavior, survival, and reproductive success
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  1. Reduced Capacity for Fatty Acid Oxidation in Rats with Inherited Susceptibility to Diet-Induced Obesity Results presented here therefore imply that reduced fatty acid oxidation is a contributing factor in development of obesity in humans and that interventions to increase fatty acid oxidation should be effective in its treatment or prevention.
  1. Phytochemicals in regulating fatty acid β-oxidation: Potential underlying mechanisms and their involvement in obesity and weight loss
  1. Antiobesity effects of green tea catechins: a mechanistic review - Journal of Nutritional article › fulltext Nov 9, 2010 · While green tea contains an array of compounds, the putative antiobesity effects have been most … [59]Friedman, M.I. Obesity and the hepatic control of feeding behavior. BROKEN LINK
  1. The Role of White Adipose Tissue in the Development of Obesity-associated Insulin Resistance and Endogenous Fat Mass Control
  1. Mitochondrial Protein Acylation and Intermediary Metabolism: Regulation by Sirtuins and Implications for Metabolic
    Disease
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  1. Diet Metabolism & Obesity
  1. Obesity, Metabolic Syndrome, and Musculoskeletal Disease: Common Inflammatory Pathways Suggest a Central Role for Loss of Muscle Integrity Obesity an inflammatory pathway? Hmmm? “…The resulting model of obesity is based on a growing body of research demonstrating that altered mitochondrial energy production, particularly in skeletal muscles, is a major anomaly capable of setting off a chain of metabolic events leading to obesity. …”
  1. The Role of Impaired Mitochondrial Lipid Oxidation in Obesity
  1. SIRT3 Deficiency and Mitochondrial Protein Hyperacetylation Accelerate the Development of the Metabolic Syndrome
  1. Hepatic CB1 receptor is required for development of diet-induced steatosis, dyslipidemia, and insulin and leptin resistance in mice
  1. A Decrease in DKK1, a WNT Inhibitor, Contributes to Placental Lipid Accumulation in an Obesity-Prone Rat Model1
  1. Mice long-term selected for high body mass are more susceptible to body fat deposition in response to a high fat diet due to insufficient increase in heat production
  1. Adipose tissue stearoyl-CoA desaturase 1 index is increased and linoleic acid is decreased in obesity-prone rats fed a high-fat diet
  1. Mice lacking angiotensin-converting enzyme have increased energy expenditure, with reduced fat mass and improved glucose clearance
  1. A Nutrigenomic Framework to Identify Time-Resolving Responses of Hepatic Genes in Diet-Induced Obese Mice
  1. Phenotype-based treatment of dietary obesity: differential effects of fenofibrate in obesity-prone and obesity-resistant rats
  1. Beneficial Effects of Common Bean on Adiposity and Lipid Metabolism
  1. Long-Lasting Metabolic Imbalance Related to Obesity Alters Olfactory Tissue Homeostasis and Impairs Olfactory-Driven Behaviors
  1. L-Carnitine Supplementation and Physical Exercise Restore Age-Associated Decline in Some Mitochondrial Functions in the Rat
  1. Differential Protein Expression in White Adipose Tissue from Obesity-Prone and Obesity-Resistant Mice in Response to High Fat Diet and Anti-Obesity Herbal Medicines
  1. Dietary fat sensing via fatty acid oxidation in enterocytes: possible role in the control of eating
  1. Fasting plasma triglyceride levels and fat oxidation predict dietary obesity in rats.
  1. Identification of behavioral and metabolic factors predicting adiposity sensitivity to both high fat and high carbohydrate diets in rats
(Ken) #3

Good validation example.

It’s “Nutty Keto Mythology” that just being in ketosis somehow magically suspends the Laws of Thermodynamics…

(German Ketonian) #4

Do I get this correctly: This means that the less hunger I feel while in ketosis (provided I am not stuffed to the rafters), the more energy my body accesses from stored fats?

(Bunny) #5

This is just off the top of my head for now!

Differences between actual fat loss & weight (e.g. like water weight). Skimming through the research DATA while posting this is that the reason some people cannot lose weight or maybe it’s fat loss like fat cells shrinking rather than actually fully disintegrating/dissipating (not sure what term to use for this?) so easily on LCHF when the body is trying to breakdown fat storage to utilize ketones is in some way related to or starting with mitochondrial processes and something to do with the skeletal muscle tissue and bone mass (not sure how to describe this one at the moment) and phytochemicals from plants or antioxidant supplementation (or some kind of supplementation from natural or man made sources) some how kicks this process in for people genetically (really hate the “bad gene” blaming thing though) or hereditarily predisposed or prone to obesity!

Those are some of the subtle clues I think Attia is referring too. Just from posting links to the research citations (have not had time read them thoroughly) the problems are becoming much more apparent and clearer to me as I skimmed through the DATA.

(Adam Kirby) #6

Yes but we have to be careful with the “laws of thermodynamics” thing because it is usually paired with some stupid ass one-size-fits-all TDEE calculation. Sam Feltham and Jason Wittrock have shown you can eat an enormous amount of “extra” energy and not put on fat mass. Did they break the laws of thermodynamics? Of course not. So to me the laws of thermodynamics are irrelevant to the discussion of weight regulation.

(Ken) #7

True, I should have clarified the context. When lipolytic and not producing large amounts of insulin, you can overeat in the caloric sense and not gain fat. My point as far as calories and thermodynamics is directed at fat loss. Once not metabolically deranged, it does apply for additional fat loss.

(A ham loving ham! - VA6KD) #8

Its important to keep in mind that the TDEE calculation is based on a statistical average of data collected over numerous studies from numerous individuals. What’s never mentioned is the variance of the individuals was as much as +/-40% …so…yeah… TDEE can be a really bad number to estimate for any individual.

(Doug) #9

I think that most times, yes, but that’s certainly a generalization. If there are no other issues, then being able to burn plenty of our own fat means our blood sugar remains more stable, and does not go low - which provokes hunger.

There are other causes of hunger, however, like the stomach’s secretion of ghrelin, and this wil vary with the individual. One can also sometimes become resistant to leptin - a hormone which suppresses hunger and which may regulate ghrelin.

(German Ketonian) #10

Got it, thanks, @OldDoug and @atomicspacebunny

(German Ketonian) #11

I think what people tend to forget is that Sam and Jason have enormously strong physiques. They have a lot of muscle and - as a corollary - very low bf%. This is not true for the Avarage Joe. I am always confused when people make this reference to Sam and Jason, hence, because this isn’t factored in. They both probably need 4500+ kcals due to their active lifestyle and powerlifting routines. Then, eating 5000-6000 kcals is no issue and additional calories are most definitely excreted (by hyperthermia, or other bodily mechanisms). If I eat 6000kcals with zc I WILL GAIN WEIGHT! Crushing 5000-6000 kcals in a day or two per week is not an issue however. So I think altering between the states of fasting and feasting is key for the Average Joe like me.

(Adam Kirby) #12

In the case of Wittrock, yes. Sam Feltham has a relatively lean, normal looking physique tho, at least in the pictures he took for his experiments. My point wasn’t that everyone will have this metabolic response, just that the “laws of thermodynamics” talking point is pretty useless for anything.

(Ken) #13

This is a tough one. Anecdotally, I’d say that when I was in a “Keto Bulk” I would routinely overeat two or three thousand calories daily and not gain fat…

(Bunny) #14

I know it’s kind of crazy because I was really really fat and pudgy before I started all this some time ago, now I can eat whatever I want and not gain fat but I do gain weight (most likely muscle mass from exercise machines and lifting weights, running with ankle weights etc.) which is not the same thing! I have super cool physique now (mind blowing enough to impress myself which is next to impossible {body image issues…lol}) but what I have noticed is that the weight has nothing to do with it (I am just stunned & stumped by it)! It makes me think the fat (in obesity) is becoming engorged with water (or something?) like some kind of bio-mechanical inflammatory issue?

Delving into this a little deeper somebody who does not exercise (muscular extertion) a lot says “I am not losing any weight or fat?” may or might be gaining muscle mass and not realize it? (I guess that’s what BMI’s and DEXA scans are for)

(German Ketonian) #15

See, I don’t know about that. The laws of thermodynamics apply with manifold error terms that the human body entails. CICO models and metabolism models both contain a portion of the truth. CICO rightly reinforces the laws, while being myopic about the human body factor, while the pure metabolism approach is too naive when it comes to the meaning of energy. At least that’s how I see it.

(Ken) #16

Interesting thoughts. I’d never considered the obesity-inflammation-water retention correlation before, but when you think about it, it appears plausable. I had significant joint and sinus inflammation when I was obese.

I can understand the Body Image issues. It’s really kind of crazy, as times I’ve been most out of shape things didn’t bother me much, but when fit, I seemed to be more aware of what I perceived as remaining faults. This appears to be fairly common, as people imagine their own faults to be glaring to other people, but are often not even noticed, or even considered a positive by others.

I’m very aware that I can still grab a small handful at my waist, but many others are not.

I do kind of doubt people not training are adding much muscle mass. Unless they previously had a nutritional defficiency.

(Bacon is a many-splendoured thing) #17

The problem with the energy deficit hypothesis (CICO) is that it requires matching your caloric intake and your energy expenditure to within something like 20 calories a day. No one can do that—our basal metabolic rates fluctuate and are affected by our caloric intake, and who knows exactly how much energy walking that extra flight of stairs really uses anyway?

The endocrine regulation hypothesis, on the other hand, makes a lot more sense, especially since the bodily mechanisms by which cells are signaled whether to burn glucose and store fat or whether to mobilize fat for metabolizing are well-documented. It’s not that the laws of thermodynamics don’t apply to the human body, but that the energy regulation systems of the body are complex and capable of handling a wide variety of conditions. Since my body does have these mechanisms, I prefer to let it handle the details, rather than bogging down my brain with complicated figuring that’s extremely likely to be wrong in the first place! :grin:

(German Ketonian) #18

That’s what I would root for as well! I agree that the endocrine regulation hypothesis overall provides orientation makes more sense, but totally ignoring energy quantities won’t be your friend either. I air on the side of the ERH over CICO any day by 70/30, roughly :wink: