Eat Less, Move mo........wha? Wait a minute

Eat less, Move more, pretty much everyone on the blogosphere is now almost universally agreed that to lose weight, you need to control calories in, calories out.

Horizone BBC had this episode a few weeks ago about exercise, in it, they show that the benefits of exercise can be achieved with as little as 3 minutes per week. What did they do? They had a guy pedal on the stationary cycle at pretty much maximum intensity for 20 seconds, let him rest a few minutes, then repeat, for a total of 1 minute spent exercising. Its referred to as HIIT in the gym goers world ( probably because you feel like youve been HIIT in the head after doing it ).

HIIT = High Intensity Interval Training.

Just do this 3 times per week, and you get all the benefits of savy gym rat.

What benefits are we talking about? Weight loss? Well no. In the show they actually perform another experiment where the reporter runs around for a few minutes and becomes completely out of breath, he is then told that he was burning on average, 16 calories per minute. Thats not even a teaspoon of sugar!

Later on in the show, we learn that the reporter's 3 minutes per week exercise did actually help him in some way, he scored slightly better in a OGTT. Thats it! Thats the REAL benefit of exercise, improved glucose tolerance. Was this exercise strategy enough to cross the lactate threshold to breed new mitochondria?

No Idea.

Anyway, I came across this video today, and at 3:12 the speaker mentions how running a marathon only burns 2600 calories. If your a well trained athlete, you can expect to complete a marathon in 2hours 30minutes, burning 17.3 calories per minute. On the other hand, if your just an average joe, you can expect to crawl across the line after about 4hours 30minutes. How many calories per minute is that? Depressingly less!

At this point I was reminded of something I saw in the comments section of this post, by blogblog, he says...

every exercise physiologist knows that exercise is completely useless for weight loss. If exercise was effective for weight loss there would be no humans because our ancestors would have starved to death a couple of million years ago. We lose 80% of our energy intake as heat. So wearing fewer clothes is a vastly more effective way to lose weight than exercise.

It appears he is right. Oh, And lets now forget how the worlds only known fat loss drug works, it doesnt mind control you and make you hit the bench press and squat rack, No. All it does is increase thermogenesis.

Eat Less Move More? Its half wrong already!. Just gotta work on that other half now.

Dopamine fat loss

Whats the connection between Dopamine and bodyfat? The answer seems to be the sympathetic nervous system.

The receptors that dopamine acts on in the brain sends a signal down the nervous system much like electricity down a copper wire to the targeted group of fat cells, whereby some triglyceride is subsequently kicked out of the central lipid droplet and is then chopped up by lipases in the cytoplasm, breaking it down to fatty acids + glycerol.

Much attention is often paid to the circulating factors in the blood that influence fat cell size, like insulin, acylation stimulating protein, epinephrine etc etc. But the connection of fat cells directly to the brain by the nervous system is often overlooked, And this connection is also reported to be a major source of lipolysis.

This paper talks about the Siberian Hamster that is seasonally obese, it is fat in the summer when the days are long and lean in the winter when the days are short. The brain is able to keep track of this seasonality by the duration of the nocturnal secretion of melatonin. However, melatonin itself does not stimulate lipolysis when cultured with fat cells.

Despite much investigation into the blood circulating hormones that where known to affect fat cell size, none of them were able to account for the dramatic change in bodyfat seen in the Hamster in response to season changes. The logical conclusion from this was that seasonal obesity was almost completely controlled by nervous system lipolysis.

It seems that in addition to dopamine, the nervous system wires coming from fat cells and ending in the brain also express melatonin receptors, and melatonin hitting these receptors triggers additional lipolysis. This is actually surprising to me, as when I was supplementing melatonin to help cope with shift work I could swear I was gaining bodyfat. I will admit though at the time that I was still eating a junk food diet, that was very insulinogenic.

Insulin really is the daddy you know.

I think this also explains why reduced sleep is linked to obesity, less melatonin reduces lipolysis, giving the chance for fat cells to increase in size the next day when you eat normally. Could it be the same principle for why dopamine blocking drugs cause weight gain? Its not that blocking dopamine causes fat storage, but rather, it greatly inihibits fat break down. The paper also mentions how blocking this nervous system activation causes less lipolsis when fasting.

Ketosis - Implications from Veech's latest paper

Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet.

Peter@Hyperlipid should hopefully be making a much more thorough post on Veech's papers in the future but in the meantime I thought id list here some interesting points and possible implications from his latest paper linked above.

Introduction

Surprisingly, Veech opens with the observation that the degree of Ketosis that is usually reached on a Ketogenic diet is, at best, "modest". He goes on to further state that almost complete avoidance of all carbohydrate calories is needed to get insulin sufficiently low enough to keep adipose tissue lipolysis high enough to fuel increased ketogenesis levels.

Recall that, the liver will in general produce ketones as fast as it can, and the only thing that stops the liver doing this is insulin and the availability of free fatty acids coming from lipolysis from the adipose tissue. Also recall, that ketones have a negative feedback loop to help control thier production rate, since adipocytes possess receptor HM74A that is suppose to bind beta hydroxybutyrate and reduce lipolysis. This same receptor also binds nicotinic acid, and is the reason that a niacin shot reduces lipolysis, at-least in the short-term.

However, insulin is required for this beta hydroxybutyrate feedback loop to work, and this is why type 1 diabetics are at a danger of ketoacidosis. When you have no or very low insulin, and lots of free fatty acids, the liver starts churning out ketones at light speed.

Further implications arise here also, there is strong anecdotal evidence amoung low-carbers that they tend to lose more weight with protein restriction aswell as Carb restriction, the so called atkins "fat fast". The avoidance of protein may well lead to even further lowering of insulin levels and thus even further increased ketogenesis. Further anecdotal evidence comes from coconut oil consumption, some people report increased weight loss and the breaking of a weight loss plateau from coconut oil, which is well reported to further increase ketone levels.

Veech has a short mention of the so-called deleterious affects of ketogenic diets, he mentions increased cholesterol, increased serum FFA, and incidence of fatty liver in mice. Hmmmm, sadly even being intelligent as im sure Veech is, doesn't always protect you from mainstream bias it seems. Pity.

Veech's team have manufactured something called a Ketone ester to help investigate the affects of high ketone levels without the complications of poor palatability on atkins fat fast diets and the so called deleterious metabolic affects mentioned above. It seems with Ketone esters, we can achieve all the benefits of high ketone levels while still eating a modest high carb diet! Good Job!

Ahem

Anyway, in the next paragraph, Veech touches on how ketogenic diets are associated with reduced weight gain and even weight loss, but he says that its unclear if this is from reduced caloric intake, or increased energy expenditure. Me personally, I would say it is both, and one of the reasons for that is increased incretin secretion. Veech mentions how Ketogenic diets do not always increase activity levels, so if there is increased energy expenditure, it may not because physical movement is higher, Veech then goes on to say that increased signalling in the PPAR receptors and increased uncoupling proteins may be the answer.

Both high-fat ketogenic and high-fat non-ketogenic diets have been shown to increase UCP1 in brown adipose tissue, but Veech is not initially sure if its from increased PPAR signialling or not.

Results

Now are are onto the experiment, where Veech's team feed mice a normal diet and a diet supplemented with ketone ester. Both diets are actually, relatively high in carbs, and without the addition of Ketone ester's, the mice in the ketone ester diet would not have had any kind of increased ketosis. Caloric content of both diets were roughly equal.

The first obersvation made was that, the ketone ester group gradually started consuming fewer calories as the concentration of ketones in the blood rise, and this is in agreement with many previous findings that in general high levels of ketones in the blood reduce appetite. This affect stabilized after 1 week, such that in further weeks, no further drop in appetite was observed.

Initially, the ketone ester diet group lost approx 12-15% of their body weight, before stabilizing at a new low nadir. The dreaded weight loss plateu! The mice were eating Ad Lib, so perhaps this can explain why people following a ketogenic diet initially experience weight loss only to eventually stall. At some point, some kind of calorie restriction could be needed to escape the nadir. Carb re-feeds also tend to work, and the reason for this is because when in deep ketosis and glycogen depleted, Carbs essentially go only towards glycogen synthesis.

Speculation here, but perhaps having a carb only day ( no protein, no fat ) after being in deep ketosis and glycogen depleted could essentially be a zero calorie day as far as your body is concerned.

Another interesting result was that, ketone levels were substantially higher at night than at daytime ( over 50% higher! ), hhmm, so if you want the benefits of high ketone levels, perhaps its better to keep your food away from bedtime. (Later on in the discussion section, Veech reports that circadian ketone levels are different in mice and rats, and that in rats, ketone levels are more or less constant, isnt it great we know so much about rodents!!!!! )

Further, the brown adipose tissue of mice on the ketone ester diet had substantially higher mitochondria content, 70% more mitochondria, and they were also 120% larger! Still further, the lipid droplets were more fragmented in the ketone group, and as we have seen here, lipid droplet fragmentation is associated with increased energy expenditure.

Looking down the results, there is a mention for our friend PGC-1 alpha, recently highlighted in the exercise study, as being the master controller for mitochondrial bio-genesis. Veech recorded 100% increased PGC-1alpha in the ketone ester group, so there is strong and direct evidence here that ketogenic diets and deep ketosis help you get new mitochondria. The workings and logic here is simple, if your demand for fat oxidation is higher, your body will make new mitochondria in response.

Another unexpected finding perhaps was that insulin sensitivity was significantly higher in the group fed the ketone ester diet, despite there still be substantial Carbohydrate in their food. But, Veech mentions how 24hr energy expenditure was essentially the same between the 2 groups and this was the reason for this similar body weights. HOWEVER, the resting energy expenditure was 14% higher on the ketone group.

Finally, its worth pointing out that Veech notes some metabolic differences in how Rats vs mice are on the ketone ester diet, and it can only make one wonder, if this difference is already so severe on 2 specie of animals that are so closely related, how much different is it going to be in animals that are even more distantly related, rodents vs humans?

De novo lipogensis is real.

Genetic control of de novo lipogenesis: role in diet-induced obesity.

Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet.

Whats up with these people thinking they can eat endless carbs and not gain body-fat? Because De novo lipogenesis is a myth? Better take a look above.

Exercise at a high intensity to get new mitochondria

Peroxisomal proliferator-activated receptor gamma co-activator-1 alpha gene expression increases above the lactate threshold in human skeletal muscle.

This study shows that exercise intensity, and not duration and/or total energy expenditure can upregulate something called Peroxisomal proliferator-activated receptor gamma co-activator-1 alpha ( PGC-1α ).

There reason intensity is important because of the lactate threshold. Once this threshold is breached, your body is like "Okay damn were exhausted, time to make new mitochondria to cope with all this lactate"

Honey has blood sugar lowering properties?

Fructose might contribute to the hypoglycemic effect of honey.

• It reduces hyperglycemia in diabetic rats and humans.
• The results indicate that fructose enhances hepatic glucose uptake and glycogen synthesis and storage via activation of hepatic glucokinase and glycogen synthase, respectively.

Whoa, was this study sponsered by the Honey industry? There has been much fructose bashing over the recent years, so they have to be afraid. Still, I never had a problem with Honey in the same way I have with starch, I do find honey kind of a more-ish food though. Still, I think its fine in small amounts as a sweetner.

low-carb chocolate ( home made)

Who doesnt like chocolate? Since im fed up of having to settle for store bought chocolate that is always full of vegetable oil and sugar, I thought id make my own version. This video is one of the top hits on youtube and his recipe is quite simple so I thought use this one with some modifications, removing that nasty vegetable oil and the insulin spiking icing sugar.

Heres what I used.....



From left to right we have, Sainsburys organic double cream, Kerrygold butter, Cocoa, Ground Almond, Nestle full cream milk powder ( only use full cream ), stevia

Ingredients:- ( this batch will contain only about 15g carbs, coming from low GI sources )

40g double cream
30g butter
3 tablespoons cocoa powder
2 tablespoons milk power
40g ground almond
25g stevia ( adjust this depending on how sweet you want it)


Step 1 - sieve the cocoa, milk powder, almond, and stevia into a large bowl



Step 2 - melt the butter and gently heat it with the cream until the butter is melted.



Step 4 - after butter is melted and mixed with cream ( on only gentle heat remember ), pour into mixture and mix away!



Step 5 - Mix throughly, then put into a dish, and put it in the fridge for a few hours! Then done!

Im not going to put up the after pictures because in this particular batch I used too much cream and it came out looking like something youd do in the rest room, lol.

Anyway, since cream and butter dont properly solidfy when cooled you will find it comes out soft and is more like fudge than block chocolate. You can use coconut oil to replace any portion of the cream and butter but it will impart a strong coconut flavor to it.

You can also vary the amount of cream and butter used to depending on how soft/squishy you want it. Another good option is to add chopped hazelnuts.

Obesity Warning! This is a HIGH REWARD FOOD and is ADDICTIVE. rrraarrgggggghhhhhh!

UPDATE:- ok I decided what the hell, put up the after pictures, NO LAUGHING PLEASE LAWL.

Fatty acid oxidation is an activated and deliberate process

Just a quick note, people need to realise that fat burning is not a passive process, something that just happens when you starve yourself or restrict carbs, it is an ACTIVATED process.

If I zap all the catecholamine receptors in your fat cells, and then starve you, you wont lose ANY body fat. It doesnt matter about calories in calories out.

You see, most of the fat in fat cells is locked away inside the central lipid droplet, like car's in a car park. They dont just "flow" naturally outside when needed anymore than car's roll out of car park's if all the roads outside are empty.

For car's to get out of car park's, you need people to drive them out, on purpose. Deliberately. In the same way, you get fatty acids out of the central lipid droplet so they can be oxidised mainly by catecholamine binding.

Perilipin, the main protein that surrounds lipid droplets, is activated by catecholamine binding, it then lets fats out of the central lipid droplet so they can be broken down by hormone sensitive lipase and other enzymes.

Perilipin is hyperphosphorylated by PKA following β-adrenergic receptor activation. Phosphorylated perilipin changes conformation, exposing the stored lipids to hormone-sensitive lipase-mediated lipolysis. Although PKA also phosphorylates hormone-sensitive lipase, which can increase its activity, the more than 50-fold increase in fat mobilization (triggered by epinephrine) is primarily due to perilipin phosphorylation

Low-carb chocolate! ( Homemade )

I took the recipe from this video however I had to modify it because

Ketosis is perfect, but 1 problem

Deep ketosis is just amazing, everytime I come back to it im just amazed at how better I feel, it keeps me in a good mood all the time, I have infinite energy, body fat disintegrates, my attention/focus and memory are better.

But theres just 1 problem with deep ketosis.

I CANT FUCKING SLEEP AT NIGHT

goddamn, why does it have to be like this?

Fat-specific protein 27 and Intermittent fasting

I was alerted to this study recently whereby Intermittent fasting upregulates something called Fat specific protein 27 ( fsp27 ) in lipid droplets.

First, what is a lipid droplet?

Its basically a car-park for triglyceride inside cells, its classified as an organelle, and its where all the triglyceride goes for long term storage. The lipid droplet is surrounded by a phospholipid monolayer along with protein linking chains, one type of the proteins is called fsp27

What does Fat-specific protein 27 do?

Well it would appear that research is ongoing at the moment, a pubmed search of fsp27 yields only a small number of reports. But what we have so far seems to indicate that it is involved in the merging of smaller lipid droplets into larger ones. If you look at this study you can see pictures of fat cells with both small and large amounts of fsp27. In the cells with alot of fsp27, the lipid droplets are enlarged, and merged. The study also reports increased mitochondria in cells that have relatively little fp27, and they have many many small lipid droplets.

I should point out though that the form of intermittent fasting in the study mentioned above was an extreme version, 3 days on 3 days off. As im aware, that is a far cry from what many people practice normally.

Anyway, another study was able to show that fsp27 knockout causes fragmentation of lipid droplets, resulting in increased energy expenditure. They have some colorful cartons to show how it works.

Horizon BBC - Truth about Fat

Horizon from the BBC are airing a new show tonight, an earlier preview from the BBC Breakfast gave a hint as to what they will talk about, in particular it seems to be about the roux-en-y surgery and how it causes dramatic increase in gut hormones that signal satiation and trigger energy expenditure.

I have blogged quite extensively on this, GLP-1 is the main hormone, also included is the fact that bile acids hyper-activate the TGR5 receptor in this type of surgery.

UPDATE:-

OK, after seeing the program I am slightly disappointed, however the doctor did mention one thing that was painfully true, "obese people generally do not feel that hungry, but when they start eating, they find it difficult to stop"

This is how I would feel all the time eating a mixed diet of carbs/fat/protein. Remember there is no receptor for calories, but we do have receptors for PYY and GLP-1, if those receptors are not activated properly after a meal, your body will not even realise that you had something to eat and will think your still starving and that a famine is going on, it doesn't matter that your 300lbs.

Why is confidence so attractive?

Because uncertainty is so repulsive!

We already saw from here that confidence is very seductive. But the looming question is, why?

Well, I reckon its because of this, as I posted on before, Ambiguity Aversion: we don't mind risk but we hate uncertainty.

Confidence is nothing more than the communication of certainty. And we love certainty, as demonstrated by the age old test, what do you want, a garaunteed £500, or, I flip a coin, if you win you the flip you get £1000, if you lose the flip, you get NOTHING. ( most people chose the garaunteed £500 )

A bird in hand is worth two in the bush.

blah blah blah.

Glucose can wreck your Beta Cells - Its Destiny

Love those dramatic titles! Anyway, new study on Carbohydrate response element-binding protein (ChREBP).

ChREBP is basically gene expression induced by carbohydrate consumption, Lucas Tufar has blogged about it here, I say destiny in the title because nuclear receptor binding is inevitable. ( aslong as your not some kind of freakish mutant ) Nuclear receptor binding is the definition of gene expression, and ChREBP is involved right at the nuclear level, right next to your DNA.

• ChREBP activates downstream target genes, including fatty acid synthase
• leading to lipid accumulation, increased oxidative stress, reduced insulin gene transcription/secretion
• and enhanced apoptosis ( wweeeeeeee, self-destructing beta cells is good for your health )
  
• beta cell-specific Chrebp overexpression is sufficient to phenocopy glucotoxicity

All of this is irrelevant ofcourse because we all know the problem is too much dietary fat.

Glucose in starvation

Just a quick post of a paper with some good info on glucose and starvation. The most interesting points are quoted below. Bite size!

Fuel Metabolism in Starvation
Annual Review of Nutrition
Vol. 26: 1-22 (Volume publication date August 2006)
First published online as a Review in Advance on May 9, 2006
DOI: 10.1146/annurev.nutr.26.061505.111258

• studying carbohydrate metabolism using C14 in liver slices from normal and alloxan diabetic rats. Fructose uptake was similar; however, labeled glucose conversion into glycogen, fat, and CO2 were all diminished in the diabetic. Insulin therapy corrected the deficiency.
• In contrast to muscle, glucose permeated the liver cell wall equally in normal and diabetic patients
• Many small points were clarified regarding adipose tissue, such as the release of free glycerol with the fatty acids mobilized during fasting or epinephrine stimulation
• But all of these studies suggested that the role of insulin in fasting is very important, perhaps as important as its role in the fed state.
• We also fasted two type 2 diabetics, who differed from the normals by better nitrogen conservation. They were slightly more efficient, in keeping with the concept of James Neel (at Michigan) that type 2 diabetes may have been an evolutionary selective advantage in a starving population.
• Three very intelligent obese subjects were selected for a five- to six-week starvation study (Figures 1 and 2). Urinary nitrogen excretion fell to 4–5 grams/day, and catheterization of the jugular, as we expected, showed some two thirds of brain fuel consumption to be D-ß-hydroxybutyrate and acetoacetate, markedly diminishing the need for muscle proteolysis to provide gluconeogenic precursors
• About two fifths of fatty acid metabolism in the whole body is via hepatic ketogenesis, some 100 to 150 grams/day. Yet there is still significant brain metabolism of glucose
• Total splanchnic glucose production in several weeks' starvation amounts to approximately 80 grams daily. About 10–11 grams/day come from glucose synthesis from ketone bodies, 35–40 grams from recycled lactate and pyruvate, 20 grams from fat-derived glycerol, and the remaining 15–20 grams from protein-derived amino acids, mainly alanine
• The kidneys in starvation produce about two fifths of new glucose.
• Next, I turn to the question of what controls hepatic glucose production. It appears simply to be the rate of release of alanine from muscle as reflected by its blood concentration
• Elevated levels of ß-hydroxybutyrate inhibit adipose release of free fatty acids (73, 81), but insulin is necessary for this effect.
• However, caloric homeostasis in a 70-kg man on protein alone is incompatible with life since the maximum rate of urea synthesis is insufficient to provide even basal calories, about 1000–1300 Kcal/day, or 250–325 grams of protein
• Veech and colleagues discovered that administering ß-hydroxybutyrate to the perfused rat heart in place of glucose increased work output but decreased oxygen consumption
• Essentially, any cell challenged by low oxygen availability or by a toxin interfering with mitochondrial function should benefit by utilizing ß-hydroxybutyrate in preference to any other substrate, including glucose, lactate, pyruvate, or fatty acids. In a very simple experiment, mice given ß-hydroxybutyrate exposed to 4% oxygen survived longer.

Anti-aging - what does calorie restriction have to do with it?

Poster Teaser made me aware of this study on lowcarber.org recently.

Born to run; the story of the PEPCK-Cmus mouse

It has some surprising implications, and ties in with my previous post. This study would seem to suggest that it is NOT calorie restriction that promotes longevity, but rather it is having a high number of mitochondria and running your metabolism on fat!

These studies focused mainly on the potential role of PEPCK-C in the generation of alanine, which occurs during fasting in skeletal muscle

Alanine is the main amino acid ejected from muscle during fasting to fuel for glucose creation to support the brain.

biochemical analysis of the skeletal muscle indicated high levels of triglyceride in that tissue. In fact, the concentration of triglyceride in the skeletal muscle of the PEPCK-C^mus mice was directly proportional to the activity of PEPCK-C in the muscle, suggesting the importance of glyceroneogenesis in the tissue.

Fat burning metabolism folks.

Skeletal muscle triglyceride is clearly the major fuel driving the hyperactivity in the PEPCK-C^mus mice; they have many more mitochondria in their skeletal muscle than found in the muscle of controls, supporting the enhanced rates of fatty acid metabolism noted in the mice.

What did I just say?

After weaning, the PEPCK-C^mus mice eat 60% more than control littermates but weigh almost half as much.

So I guess that means thier running a fast metabolsim and should live relatively short lives, right?

A second surprising result was the apparent extend longevity of the PEPCK-C^mus mice; they lived almost two years longer than the controls and had normal litters of pups at 30 to 35 months of age (most mice stop being reproductively active at 12 to 18 months).

Whoops, guess that theory is out the window now.

levels of hormones and cytokines in the blood of the PEPCK-C^mus mice and noted very low levels of insulin, leptin and MCP-1 as compared to control animals

Low insulin. They say in the study that the low leptin is because they have very low amounts of white fat mass.

We suspect that the major factor responsible for the longevity of the PEPCK-C^mus mice is the very low concentration of insulin in the blood of the mice that is maintained over their lifetime of hyperactivity.

Yeh so what was I saying, low insulin.

Anyway, the only question mark in this study is, what is driving the mice to be excessively active? Is it the fact they have a large number of mitochondria? Or is the fact that overexpression of PEPCK-C results in increased cleareance of citric acid cycle waste products?

Adiponectin implicated as initiator for the benefit of Calorie Restriction

Serum from Calorie-Restricted Rats Activates Vascular Cell eNOS through Enhanced Insulin Signaling Mediated by Adiponectin.

Laser surgery to spot reduce fat

Came across this article today in newspaper,

They are using laser treatment to make targeted fat cells spill their contents, their website explains how this works......

Paddles are attached to the specified area of the body and a low class laser is used to penetrate just under the skin to break down the underlying fat cells. When the laser hits the fat cells, pores form on the cells and they release water, glycerol and fatty acids. The fat cells reduce in size.

The lymphatic system then removes the glycerol and fatty acids through the venous system where they are processed in the same way as fatty foods that are digested. It is therefore crucial that clients exercise after treatment to metabolise the fatty acids.

The treatment does not affect any of the surrounding structures such as the skin, blood vessels or nerves.

They recommend 45 minutes of heavy cardio after treatment to burn the fats, which makes sense I suppose, but it does arise the question, if the fats re-enter the system as though they had just come from digestion, Do they go back to the cells they came from if you don't exercise? And if so, how is it that the fats "know" where to go?

Also, its been shown time and time again that exercise burns only insignificant amounts of substrates, how is it that only 45 minutes of exercise is sufficient enough to oxidise all this fat that's been forcefully ejected?

In the picture in the newspaper article, the before and after pictures are shown, you can see in the after picture her stomach looks slightly wrinkly, which is the classic sign of fat cell atrophy.

These fat cells will be very small and thus very insulin sensitive, what's to stop the fat therefore preferentially coming back to this area since these fat cells are relatively hyper-sensitive to insulin?

If the fat doesn't easily come back after treatment, then I think this is indeed good confirmation of the theory that fat cells do not passively uptake circulating fats for long-term triglyceride storage, but instead the process of triglyceride synthesis is activated and deliberate.

The fact that subcutaneous insulin injections cause localised fat cell hypertrophy is again further support for this theory, with it pointing to insulin as the culprit.

Stevia vaporized my sweet tooth

Ive always had quite a voracious sweet tooth, its one of the reasons I always fall off the low-carb bandwagon and regain weight after a loss.

Stevia, the natural sweetner from the plant was recently approved for sale here in London and I thought it would make a nice additional to my home made hot chocolate.

The smell is very strong, its very much like caramelised toffee, it doesnt "taste" like sugar but it is very sweet. The best part though is it has completely annihilated my craving for sweet stuff. Just half a teapsoon in a glass of water and BOOM, I completely go off sweet things for the rest of the day.

Its also fantastic with a can of coconut milk, if you buy a brand of coconut milk thats quite watery ( should be about 5.5g of fat per 100ml ) , mix in 1 teaspoon of Stevia to sweeten and its the PERFECT low-carb ketogenic drink. Its low in protein, low in carbs, and the best part is its also quite high in minerals.

Adipose tissue stores glycogen - I told you to watch those carbs Joe!

Oh oh oh, this is interesting. How the fuck is it that no-one talks about adipose tissue storing glycogen? Its all making sense now, remember all those studies showing how insulin resistence in adipocytes makes you lean and mean, WELL NOW WE FUCKING KNOW WHY!

Enhanced glycogen metabolism in adipose tissue decreases triglyceride mobilization.

Stranger in a strange land: roles of glycogen turnover in adipose tissue metabolism.

Both these studies are free full text, going to read over them and update this post when ive made my own conclusions.

UPDATE:-

OK having read both the studies there isn't anything that novel or interesting. The authors are very quick to always point out that ultimately, calories in / calories out is what matters most, hinting at a possible underlying bias.

The only unexpected finding was that elevated glycogen levels in adipose tissue significantly inhibits triglyceride hydrolysis.

Nuclear receptors - something no-one talks about

I think if you ever wanted to know what "gene expression" exactly is, look no further than nuclear receptors. You have receptors around your DNA nucleus in your cells that bind different things, this basically causes activation of your DNA to produce difference proteins ( polypeptides is a better word ) , thus expressing different gene's. !!!!

Sustained activation of PPARα by endogenous ligands increases hepatic fatty acid oxidation and prevents obesity in ob/ob mice.

PPARα is nothing other than simply a certain receptor sported on the nucleus of mainly your liver cells. And it binds fatty acids. I havent so far been able to find a comprehensive list of ligands but PPARα is reported to be responsible for the fasting response.

PPARα activation also reverses fatty liver. yay!

In the study above the researchers manipulated some enzyme called Peroxisomal acyl-coenzyme A oxidase 1, basically turning it off, such that PPARα was excessively activated, the result was a lean rodent. ( even though this rodent is genetically predisposed to be fat )

However it seems there was a price to pay, all the extra fat burning in the liver resulted in oxidative stress overload and liver cancer.