Friday, 27 July 2012

Calorie restriction can increase fat mass

So says the researchers from this study. All the people trying to lose weight by following some kind of "mild calorie restriction" may actually be setting their physiology for increased fat gain in the future.

Its nothing complex, its simple actually. Body senses food shortage = adapts to environment by increasing fat storage to cope with future uncertainty. Thats what biology does you know. It ADAPTS. I think they call it evolution.

Literally every animal study ive seen shows weight regain and weight rebound after a period of calorie restriction. If the calorie restriction is severe it will force temporary decreases in fat mass while the calorie restriction persists, thats just more physics than biology. However many people pretending to be intelligent will think that is how to treat obesity.

Ofcourse calorie restriction is really incretin restriction. Thats whats really going on. As I have said many times, the incretin affect is the only way your body is able to determine current food availability in the environment. Leptin has a similar role, it tells the body about current reserves of fat stores that are already in the body. In a normal human the incretin response is suppose to be directly proprtional to calories ingested, however as we have seen it is broken in both situations of very low adiposity and high adiposity. In anorexia, the incretin response is over-exaggerated while in obesity the incretrin response is depressed.

As we know Roux-en-Y gastric bypass (RYGB) is one of the most effective "treatments" for obesity as far as producing weight loss goes, and there is considerable evidence to suggest it is only affective because it goes some way to restoring the incretin response. Up to 20% of patients cannot sustain their weight loss beyond 2 to 3 years after RYGB surgery. Weight regain-promoting consequences are attributed to a failure to sustain elevated plasma PYY concentrations ( 1 )

Tuesday, 24 July 2012

Away with you caffeine

I was recently mortified to learn that one of my lifelong addictions ( diet soda ) is actually LOADED with caffeine. I had been drinking large amounts of pepsi max for years but recently I have noticed that my consumption of this stuff had gone to ever new dizzy heights, I would easily go through 5 cans per day, or 2 litre bottles. Im disgusted with myself.

1 can of pepsi max has a reported almost 70mg of caffeine!!!! In conjunction with the other stuff I was drinking I now realise I must of been getting easily over 500mg caffeine per day. Suffice to say, my sleep was getting worse and worse and worse. Last week I decided enough was enough and I needed to take drastic action and go cold turkey on caffeine to help improve my sleep. I couldnt function anymore, I do not exsist without a good nights sleep.

Anyday where the sleep is bad is a completely wasted and substracted day from your lifespan, because without a good nights sleep I literally become moribund. There are some interesting things in the wikipedia page on caffeine, its consumed by like 90% of people, and over 250mg you can start to develop symptoms of something they call caffeinism, rofl thats NOTHING compared to what I was consuming. IT makes me wonder now how all these problems people have in society with bad sleep may be atleast partially the result of caffeine intoxication.

I have been caffeine free for 8 days now, first 2 days were quite easy, days 3-5 I had very very bad headaches and on day 6 I was literally bed confined for 24hrs with the worse head ache ive ever had. However my sleep has been gradually improving. I have been dreaming more and feeling a bit more freshed upon waking. In short, I can LIVE. Despite my shift working already fucking up my sleep, the caffeine intoxication on top of this was murdering my brain. I know dreaming is linked with REM sleep, so Im sure ive been getting more REM sleep while off the caffeine.

Infact REM sleep is oh so important. I know this from my experience with zopiclone which I use to help cope with my shift work. I only take zopiclone once every 8 days to avoid addiction and dependence, but tbh thats all I need. Anyway the science literature has done extensive work on zopiclone and one of the things it does is give you almost no REM sleep and instead you get all slow-wave sleep.

I know exactly what this feels like because after zopiclone I wake up with my body feeling highly refreshed and ready to go, but my brain and cognitive acts exactly like I didnt get any sleep at all. Now with the caffeine out I can just feel im getting more REM sleep because the front of my brain doesnt feel heavy in the mornings.

Ive gone cold turkey on caffeine and now I swear to god im never going to consume it ever again. ( except from chocolate HAHA ),

No more diet coke/pepsi, no more coffee. I dont need that shit in my veins. All these studies supporting the benefits of caffeine just make me laugh and cringe at the same time. WHAT FUCKING BENEFITS?! I can send my poor brain into over drive, get less sleep, consume more caffeine, go more into over-drive, just so I can function "normally"?! How about just getting a good nights sleep and functioning normally that way?!?! I dont need plant insecticides to work normally thanks. Which brings me to the next point....

Why do manufacturers put caffeine in their products anyway?

There is only one answer, and thats because it increases sales. How does it increase sales? Because its addictive. I speak from experience, remember paragraph 1 above ^^ . Although caffeine is quite an easy addiction to give up, you wont ever realize it until your sleep is so shit that your on your knee's begging for release. I even found a review paper on pubmed suggesting that caffeine may worsen glucose tolerance and aggravate hepatic glucose production.

That does it!, away with you caffeine!


Monday, 23 July 2012

London property overpriced

A decent 2 bedroom flat in London would set you back £250,000, with price fluctuations depending on area, infact you may have to go up to £350,000 for a 2 bedroom flat. But hell, lets use the lower end of the price bracket for arguments sake.

To demonstrate how overpriced this is, lets compare it to gold, not worthless fiat.

A 1kg bar of gold costs £33,000 , rounded down.

This means, in theory, I should be able to trade 7 and half bars of 1kg gold for a 2 bedroom flat. Now just pause and think about this for a moment. Can you envisage yourself handing over 7 and a half massive pure gold bars in exchange for a measly 2 bedroom flat that doesnt even have a great deal floor-space?

Maybe im crazy, but it seems that 7 and a half gold bars should buy you substantially more than a 2 bedroom flat like that. 7.5kg of pure gold is a HUGE amount of gold, much more than most people will ever see in their lifetime, let alone own and be able to trade for a house. Can you imagine what would happen if housing did not sell for £££ but rather could only be bought for with gold.

Every guy in the land hoping to start a family would have to turn up to their estate agents carrying bags of gold bars to get a house. But just one second, WHERE THE FUCK IS ALL THAT GOLD GOING TO COME FROM?! The UK gold reserve is only 310 tonnes, or 310,000 1kg gold bars. Divide that by what 2 bedroom flats are worth and you get 41333.

So even if we raided the UK gold reserve, only 41,333 men would be able to afford 2 bedroom flats. According to the census, the UK population is 62 million, lets half that, and we get about 31 million men in UK. But only 41,333 guys in that 31 million can afford to buy property??? We can only count 2 bedroom+ flats because that is the minimum needed to start a family, you cant start a family in 1 bedroom flat.

Anyway, something is wrong. Either gold is way way underpriced, and/or London property is hyper-inflated. Actually I think its BOTH.


Wednesday, 11 July 2012

Ketosis and adiponectin - there is a link!

Some discussion on the recent post by tom naughton on the interview with Dr Phinney. I questioned some of Dr Phinney's points on that forum about the importance of serum ketone levels.

Dr Phinney argues that it takes weeks to "keto-adapt" and that the serum ketone levels are very sensitive to not only carbs but also protein in the diet. I think most people knew this, that protein affects serum ketone levels not just carbs. Dr Phinney argues that a low-carb diet must also be a very high fat diet, something which I certainly agree with. But I wasnt to sure on the affects of differing serum ketone levels could have.

Anyway, shortly after I stumbled on this paper which is a big piece of the puzzle. Basically what this says is that beta-hydroxybutyrate stimulates adiponectin secretion through the GPR109A receptor. ( ignore the stuff about niacin ).

Check out the wikipedia page to get a glimpse of how beneficial adiponectin is to health.

So now the picture is very clear, high fat diet along with low carb and low(ish) protein not only results in high glp-1 secretion but also high adiponectin secretion due to high levels of serum ketones. Both glp-1 and adiponectin are very important for curing metabolic syndrome.

Transgenic mice with increased adiponectin show impaired adipocyte differentiation and increased energy expenditure associated with protein uncoupling.

Ah ha! Adiponectin suppresses adipocyte differentiation, what this means is that high levels of adiponectin directly inhibits fat tissue growth! bingo! And it makes sense, high serum ketones is a marker of starvation, and fat tissue growth is the last thing you want when your starving!

Friday, 6 July 2012

Anorexia and incretins - your still not in control

There is an underlying biological basis for all so called mental/psychiatric disorders, people do what their biology commands them to do, there is no "willpower".

This study looked at the PYY response to meals in normal people and people with anorexia. Recall that PYY is a potent satiation hormone secreted from the gut, it tells you STOP EATING, and it shifts your attention away from food and hunger. In the graph below we see that not only do people with anorexia have elevated baseline PYY, the response of PYY after a meal shoots up off the scale almost. What does this mean?

It means that people with anoerxia are told by their bodies to curb food intake, contrast this to an obese people, that typically has a much reduced PYY not only at baseline but in response to food.






Thursday, 24 May 2012

Back on the IF bandwagon - and its working

After the rodent study I decided to get back on the IF bandwagon, especially given what we also learnt about diurnal cortisol in the same post. The biggest point about diurnal cortisol is not to eat for atleast 3-4 hours after waking up, let the cortisol come down before you start munching on grub.

Anyway, I have been doing 23/1 IF since, and I was pleasantly surprised that my glucose tolerance was considerably higher. In line with diurnal cortisol, I have been waiting until 4pm-6pm in the evening and then consuming all my calories in one large meal, ive even been sneaking in some carbs in the form of candy and banana's. Im also taking 1000mg metformin with the meal, and pre-loading with 2 teaspoons of white wine vinegar.

I dont restrict myself, I dont count calories, I just eat whatever I want and eat to hunger. My estimate is it comes out to about 2200 calories.

My plan was to continue this for a few days until I became accustomed to the circadian rhythm of feeding, and then transition more into a ketogenic diet but still keeping the 23/1 feeding pattern. I needed to eat higher carb and bit of junk food in the beginning to keep myself satisfied and not strain myself with cravings while my body adjusted to the new 23/1 pattern because ghrelin is also on the circadian clock and it takes time to adjust. Eating ketogenic on 23/1 will inadvertently lead to reduced calorie intake because it wont be easy eating 2200 calories of low-carb in one meal, not unless I start drinking pints of cream.

OK, so yesterday was my first low-carb day on the IF 23/1 and today I had some comments from work colleagues "hey it looks like your losing weight", tbh my trousers do feel noticeably looser. Great! I never weigh myself on the scales because its just playing mind games with yourself, I just go by how I feel and how my clothes fit. I actually did 23/1 back in 2007 and looking back now I remember that's when I also managed to get down to my lowest weight, alas, everything literally went "pear-shaped" though when I started my new job and came under stress and pressure.

Stress and depression make me crave sucrose laden foods. This has been the prime reason I have yo-yo dieted so much. Sucrose is how I artificially raise my mood to cope with stress and depression. Although sucrose tends not to make me gain weight in small amounts, once I get the mood high from sucrose foods I end up binging on huge amounts and its very hard to pull myself away from it.

I cant eat just one strawberry lace or just one drumstick lolly, as soon as I get the taste of sucrose on my tongue I just get completely mind-controlled and consume it all. I.E. hyperphagia , Fruit does not have the same affect at all. Only human engineered foods cause these addictions.

I want to quickly comment on something else aswell, Today I had only bacon and eggs for my meal. Anyway about 30 minutes after the meal I got very drowsy, and it was lights out, I must of napped for about 1 hour. This is post-prandial somnolence, and I was surprised that this happened because I had assumed this phenomenon was primarily a function of the tryptophan:LNAA ratio in the blood, and that only high carb meals that spike insulin were capable of post-prandial somnolence by shunting more tryptophan into the brain.

Sigh, so thats another theory out of the window. Unless the egg white had something to do with it? I ate 4 egg whites in the meal, and egg whites are high in tryptophan ( but they are high in BCAA aswell! ). This study used something called hydrolysed egg protein to raise the tryptophan:LNAA ratio. No idea what that is, and it probably isn't the same as fried egg whites. So meh.

Anyway, the rodent IF study has finally nailed it into my brain, that when you eat is likely just as important as what you eat. I'm sure I wont stay 23/1 forever, but I will keep the lessons that rodents teach us in mind. 23/1 is good for weight loss, and I will probably resume 2 meals per day in a 6 hour window in the future for maintenance.

hhhhmmmm, im sure the government nutrition guidelines of eating 3 meals per day must be causing more harm than good.



Sunday, 20 May 2012

high CHO vs high FAT dieting

I stumbled across this old paper ( 1964 ) recently, sometimes these old papers can be real gems because the scientists of old were probably less influenced by bias, political correctness, and corporate/financial motivation. I dont have access to the full paper which is a shame, so im left with decrypting the abstract. BEWARE! He talks about mice again. Extrapolate to humans at your own risk!

The rate of weight loss in mice produced by restricting calorie intake below normal requirements is influenced by the type of food predominating in the diet; fat producing a rapid loss and carbohydrate a slower one.
I.E. a calorie is a calorie.

oh wait..

The amount of weight loss in both instances can be accounted for almost entirely by the extent of the negative carbon balances.
This is just basic common sense. To lose weight, you must expelle more carbon atoms than you ingest.

The varying rates of weight loss are due to differences in the rate of fat loss and not to changes in total body water.

Dont listen to this guy!, common knowledge is right, you only lose water on atkins diet!

In mice on a normal diet and in carbon equilibrium, about half the carbon is excreted as CO2 and half in the form of organic molecules with an energy value of their own.

I.E. the body wastes calories. This is why its foolish to talk about energy balance and calories in calories out, it only makes sense to talk about carbon balance.

With restricted calorie high carbohydrate diets the proportion excreted as CO2 rises to over 80 per cent of the total while the proportion excreted in the form of complex molecules falls.

What this basically says is that on a low calorie high carb diet, your body becomes EXTREMELY efficient, and most nearly all carbon atoms are completely oxidated to CO2 before being expelled from the body. Being efficient is not something you want if your to trying to reduce something. ( fat mass )

With restricted calorie high fat diets the proportion excreted as CO2 remains normal. The half excreted as complex organic moleceules is significantly altered as to its distribution between feces and urine.

Now this is a tricky statement to dissect without the full paper. We know that ketones are excreted in breath and urine on a ketogenic diet, but whats this stuff about feces excretion of carbon atoms? Can you shit out calories? Maybe it only happens if your a mouse?

With restricted calorie feeding the proportion of food and/or tissue totally degraded to CO2 influences the amount of energy available to the organism.
I would re-word this to "with restricted nutrient feeding". Total calories consumed are not so as important as amount of carb/protein/fat consumed. Things make more sense when you consider the next statement....

The demands on its own fat stores are consequently greater when fat is the major constituent of such a diet.
Again the way I would look at this is that, "the demand on fat stores is greater when protein and carbs are only very small parts of the diet". It does seem to me that researchers are hesitant to admit when the calories in calories out model fails to predict something. Remember the monkey study where the researchers lost some calories?

This next paper is a good example of that.....

The role of energy expenditure in the differential weight loss in obese women on low-fat and low-carbohydrate diets.


We have recently reported that obese women randomized to a low-carbohydrate diet lost more than twice as much weight as those following a low-fat diet over 6 months.
All lies, a calorie is a calorie.

The difference in weight loss was not explained by differences in energy intake because women on the two diets reported similar daily energy consumption.
Remember we are scientists! And calories in calories out is a universal truth and law! it must be obeyed at all time! If the groups had the same energy intake, the low-carb group must of had higher energy expenditure!!!!

We hypothesized that chronic ingestion of a low-carbohydrate diet increases energy expenditure relative to a low-fat diet and that this accounts for the differential weight loss.
Yuh, because, calories dont vanish.

So anyway, after this the scientists measure various energy expenditures including basal metabolic rate ( which we have already seen does not predict adiposity ), thermic food affect, and physical activity. The researchers had this to say next....

Mean REE in the two groups was comparable at baseline, decreased with weight loss, and did not differ at 2 or 4 months. The low-fat meal caused a greater 5-h increase in TEF than did the low-carbohydrate meal . Estimates of physical activity were stable in the dieters during the study and did not differ between groups.
OK, OK, that can ONLY mean one thing!, food intake was the same, energy expenditure was similiar, so that means.......................................drum roll

The differential weight loss is not explained by differences in REE, TEF, or physical activity and likely reflects underreporting of food consumption by the low-fat dieters.
I.E. fat people are fucking liars!!!!