Sunday, 12 February 2017

Atkins fat fast is hard

Ive been toying with the Atkins fat fast protocol recently, and I must say it is far more difficult than you might realize. Even eating 2000 calories a day of mostly cream, nuts, avocado, there is an underlying perpetual hunger that calories alone cannot seem to satiate. Over the years ive become very good at recognizing the hormonal and instinctive urges my body conjures and I know what this hunger is, it is hunger for protein.

This is a very good anecdote for the "protein leverage" phenomenon which I have no doubt is absolutely true. Protein causes the release of a different set of hormones ( PYY for example ) from the intestine than fat that interacts with the vagus nerve and this is what satiates and turns off appetite.

My interest in the fat fast was rekindled after seeing this study tweeted...


Subjects were made to compare their weight loss on fasting for 10 days to eating a fat fast style diet ( 82% fat, 14% protein ) of 1000 calories for 10 days. Thats about 35g of protein per day for reference,  just slightly more than a single chicken breast.

So what happened?

The data show that the weight loss while fasting was 64.6% due to loss of lean body tissue and only 35.4% due to loss of adipose tissue. In contrast, the weight change while on the high fat diet was only 3% due to lean tissue loss and the mean total amount of body fat lost exceeded that of fasting (6.4 kg versus 3.4 kg). These results suggest that although clinically desirable weight reduction occurs during fasting, it is at the expense of lean tissue, which is physiologically undesirable.

Let me say that again, more fat is lost on 1000 cals (82% fat) per day than completely fasting. During fasting there is a disproportionate loss of lean(protein) mass,

Im not exactly sure what is going on here but I have an idea. It might be due to PPARa and hepatic amino-acid degrading enzyme ( AADE for short)

Still one of the more fascinating studies ive read comes from Semenkovich CF. , here they deleted the fatty acid synthase enzyme only in the liver,  to find some interesting results. Mice fed a zero fat diet developed hypoglycemia and when they fasted these mice they displayed characteristics equivalent to PPARa knockout mice, I.E. low ketosis and a lack of hepatic fat burning. More importantly, feeding the mice dietary fat seemed to rescue them.

The conclusions from this study are this, body fat released from adipose tissue during fasting is unable to activate PPARa in the liver, instead, a special "activator" molecule is needed that normally would be synthesized from the FAS enzyme. If you do a little digging beyond this paper you can find that one such molecule is Oleoylethanolamide. This explains why feeding the mice dietary fat also rescued them from signs of PPARa deficiency because OEA is also synthesized in the intestine from dietary fat.    

This last bolded part is probably quite important because it doesnt seem like OEA is synthesized in hardly any other tissues except liver and intestine.

Even more intriguing, a recent study has attributed some of the appetite lowering effects of gastric bypass surgery to increased synthesis of OEA in the gut.

OK OK!

so whats this got to do with the more fat loss and less lean mass lost on the fasting vs keto diet mentioned earlier?

Well.....

Hepatic Amino acid degrading enzyme is down-regulated by PPARa ( link1 , link2 ) and the second link there even mentions PPARa acting as a metabolic switch between protein burning and fat burning. Dietary protein on the other hand increases the expression of AADE, so the more protein you eat, the more you burn protein. ( and thus interrupting fat burning )

Im not sure if dietary protein directly down-regulates PPARa, but many people report lower ketosis with increasing dietary protein on a general low carb diet, so this is strong evidence that it does.

All in all, a possible contributing factor to the increased fat loss and protein sparing on a 82% fat diet compared to total fasting could be due to these interactions, I.E. unlike fasting, with dietary fat intake on the 82% fat diet there is increased synthesis of OEA ( and probably other Ethanolamide's ) in the gut which in turn helps activate PPARa . which encourages fat burning and ketosis, and lowers ADEE, which lowers protein burning. ( sparing your muscles )

Although a normal person doesnt have hepatic FAS loss and so can activate PPARa in the liver while fasting, it could well be even higher with increased OEA synthesis from the gut from dietary fat.


The last nagging point that I dont have an answer to is, why on earth is there also greater fat loss on the 1000cal diet compared to fasting?  Theres probably a whole host of reasons but it seems like consuming dietary fat ( i.e. atkins fat fast ) heavily changes your metabolism to fat burning as opposed to a mixture of protein and fat burning when fasting.

When kekwick and Pawan investigated this increased fat loss in mice their explanation was that fat was not being completely degraded to co2 before being excreted therefore reducing its caloric value.








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