I chat to a lot of people about diet and myths and facts... for example eggs give you cholesterol, all carbs are bad etc... My knowledge is limited by the research I read and the books I skim through. I try to explain the way cortisol works, insulin works, sat fats and testosterone works - and whilst I understand it to a certain point I thought it would be fun to list out all the myths and facts that we know and maybe debate them?

There seems to be many conflicts around, like test is boosted by sat fats, but sat fats contain cholesterol, cholesterol lowers test etc...

Metabolism "I have a slow/fast metabolism"... from what I understand in general metabolism is pretty much average for most, and people's metabolisms are linked to the their lean body mass and physical activity?

I've got several books by anita bean and dr john little doug mcgouf all quite interesting but some go into too much pointless depths and some just scratch the surface.

We have a lot of experts on this site so I'd be keen to hear your myths and facts - maybe we can build a bit of a diet "database" or factbase that we can point people to in future?

You can have a fast metabolism, I can lose a stone sitting on my arse in a week if I eat wrong. I don't think this is a myth at all, people have varing hormonal levels that affect fat loss and amount of calories burned at rest. Rabs bulking diet is my cutting diet, his cutting diet is starvation and a quick death for me and I'm definatly no bigger.

Craig wrote:You can have a fast metabolism, I can lose a stone sitting on my arse in a week if I eat wrong. I don't think this is a myth at all, people have varing hormonal levels that affect fat loss and amount of calories burned at rest. Rabs bulking diet is my cutting diet, his cutting diet is starvation and a quick death for me and I'm definatly no bigger.

LOL! Cool, now you see we already have differing opinions which is great. It's just the sort of thing I'm interested in. I just remember reading somewhere ( can't remember where) that metabolism was in a bell curve sort of distribution, that the majority of people fell under that category - and that hypo and hypermetabolisms were rare. I can understand that variations in hormonal levels will affect metabolisms,. but surely one's body works pretty much teh same as another's?

Im very like Craig. If i miss a few meals over a week ill drop weight like shit off a stick

I go on holidaym eat crap, drinke tc and come home the best part of a stone lighter

A diet myth ive found is that fruit is bad.....including eating bananas whilst dieting. fuk all wrong with a banana

Will wrote:

Craig wrote:You can have a fast metabolism, I can lose a stone sitting on my arse in a week if I eat wrong. I don't think this is a myth at all, people have varing hormonal levels that affect fat loss and amount of calories burned at rest. Rabs bulking diet is my cutting diet, his cutting diet is starvation and a quick death for me and I'm definatly no bigger.

LOL! Cool, now you see we already have differing opinions which is great. It's just the sort of thing I'm interested in. I just remember reading somewhere ( can't remember where) that metabolism was in a bell curve sort of distribution, that the majority of people fell under that category - and that hypo and hypermetabolisms were rare. I can understand that variations in hormonal levels will affect metabolisms,. but surely one's body works pretty much teh same as another's?

Not at all really, see how low carb diets suit some and for others it does nothing but strip muscle, there are so many factors involved in fat loss and muscle building that I can not begin to comprehend why anyone would say we are mainly the same........... unless they are trying to sell a one size fits all program.

Thats not to say that the slow metabolism thing is not an excuse for many but I know a fair few people who can go on a startvation diet and only lose a pound or two a week. The same for me would equal a stone in one week.


If the metabolism thing is wrong then so is body typing. We all accept that endomorpths and ectomorphs exist as we see it all the time at the gym, everyone has some guy or girl at their work that eats chocolate and crisps all day and is anorexic thin. Genetics for muscle growth is firmly accepted, why not for fat and general weight loss?

high fat diets all the way along with pre-exchaustion!

LOL^^^

Also....low fat, moderate carb, high protein diets are no good for dieting.

Depends on what you class as dieting and moderate carb.

If you're talking comp prep then probably not but for those looking to take the weight off gradually and have the capacity for the weight to stay off then it's not a bad option if you're in slight calorie deficit.

Nice thread.

Was just talking to someone about the cholesterol myths that are about... quite a few. The main thing is the circumstance in which dietary cholesterol is actually problematic - it' only might be so in very specific circumstances.

Firstly, about 80% (IIRC) of dietary cholesterol never gets into your bloodstream at all - it goes direct from the intestine to the liver where it gets converted to bile and sent straight to the gall bladder. From there the bile is used as an essential part of digesting long chain fatty acids... so on a high fat diet, you actually want decent levels of dietary cholesterol to help digestion of the other fats you eat.

Where dietary dietary cholesterol is a problem is when part of an otherwise relatively low fat diet - this leads to excessive build up of bile salts in the gall bladder and gall stones and can permanently damage your future ability to digest fats.

The other bad situation is if your serum cholesterol is way to high and already problematic for other reasons, and that 20% of extra cholesterol from diet will compound the pre-existing problem. For healthy individuals no issue.

As for metabolism there are definite large physiological differences between individuals... just body shape can have a big effect - if you take two equally healthy individuals of the same weight but different height, the taller skinnier individual will always have a faster metabolism and more thyroid output. This is due to the taller person having a body mass to surface area ratio that gives them more surface area to lose heat from... this means more thyroid generated to burn more calories at rest to maintain body temperature.

The accepted normal range of thyroid levels is huge - the top of the normal range is about ten times higher than the bottom of the normal range.

Then there's the effect of exercise frequency and itensity on resting metabolic rate, lifestyle factors and their effects, the differing thermic effects and post prandial hormonal effects of different foods... and you can't really even measure that perfectly by closely watching macros because many of the effects differ between individual fatty acid ratios and individual amino acid balance as well as type of and Gi rating of carbs... if you were a highfat/low carb dieter ate a little over 100g of fats a day in the main getting most of them from either omega 6 fats, saturated fats or monounsaturated fats or took an equal blend, each would have very differing effects on your insulin sensitivity, whole body inflammation levels and fat burning/storage efficiency, and the difference even exists between specific fatty acids within the grouping.

The effects of different balances of these things is definitely strong enough to be considered physiologically significant for effects on metabolism, hormonal balance, body fat management and even health, but because its not all fully understood, and because the overall effect is always a sum of all other factors outside of diet too there's just no way an intelligent informed person could say they know all there is to know about this and that one diet will work best for everyone.

Is damn complex and I think that however interesting it is, it's often better in the end to find what works for you by self experimentation and practical experience rather than the science books which can just drive you crazy, especially as there are so many dogmatic so-called diet experts out there who hav made their mind up already and are selective in how they look for and present scientific information about it all. Openmindedness, experimentation and honest self appraisal are your best tools to finding your optimum nutritional plan imo, and the most trustwothy experts are the ones who don't give sweepingly generalised answers.

I typed up a bit of research I was doing on this on facebook - this is what I came across in terms of cholesterol:

cholesterol is either obtained from our diets (to a lesser extent) or synthesised in a variety of tissues within the body, including the liver (yet again!), adrenal cortex, skin (believe it or not), intestine, testes, and aorta. High levels of cholesterol in your diet actually suppresses synthesis in the liver but not necessarily in other tissues... it's complimicated

Insulin has potential role to play with cholesterol as it's a pro-inflammatory hormone, which in combination with high glucose levels results in more oxidative damage to tissue. As a result a generalised inflammatory state is created typically marked by inflammations on the walls of blood vessels. Cholesterol is basically the plugging agent/concrete/mortar of the body and is found everywhere within the body. The cholesterol is there to patch up the inflammation. When the body needs to take cholesterol out of the blood stream to do this LDL is perfect as it hovers on the "outside" of the blood vessels, and HDL in the middle. IT's the LDL that is the "mortar" that sticks to the blood vessels to fix them. But if the body needs cholesterol to go back to the liver, insulin is transported via HDL instead as it floats in the "middle" of the blood stream. Hence the ratio of HDL and LDL. (High density, low density) is a good way of working out your body's inflammatory state. Restoring insulin sensitivity decreases that systemic inflammatory state, which results in less inflammation of the vessel walls therefore needing less cholesterol to be transported for this purpose on LDL molecules.

So high cholesterol is more of a symptom than a cause of cardiovascular disease. Correcting the underlying problem of high cholesterol is better than any cure, pills or anything else. Else it'll come back and you won't really have addressed the root cause of the problem. By addressing the issue the production of HDL becomes stronger and as such the ratio turns back into favourable areas.

The inflammatory state is largely but not solely related to the amount of circulating glucose and insulin in the body!

Reducing cholesterol isn't just following a hunter-gatherer type of diet with little to no carbs or any refined carbs. But also high intensity exercise/work - to deplete glycogen stores. However glucagon is nonamplifying, i.e. it's 1 for 1. So one molecule of glucagon will affect ONE molecule of glycogen. By doing high intensity exercises (HIIT being a good example), it aggressively empties glycogen, creating an enhanced insulin sensitivity situation as it becomes necessary for the body to be in that state. So you have to work at a high enough intensity to promote glycolytic cells to release their glycogen cells - and the reason it requires high intensity is that for any level of glucose ingested the amount of insulin that has to be secreted is much much lower. So the more sensitive you become the quicker your glucose metabolism becomes, ergo, your body becomes balanced once again.


As for the thyroid I also did some bookworming but clearly it doesn't cover genetic weaknesses or baby's born with actual thyroid deficiences and what I came across was 1000pages of information which was too overwhelming for me - but this is what I understood of it.

The body's temperature should be around 36C and 37C, it's the thyroid hormone's job to regulate that body temperature. A person with high fat, will have a larger surface area, and also have more insulation insulation as a result. (Basic thermodynamics, about losing heat/absorbing heat). Therefore owing to this principle, the thyroid has to compensate, else they will be overheating and therefore die. This strain lowers T3 and T4 thyroid hormones, which lowers their thyroid production. It's not necessarily because they have a bad thyroid that they're getting fat, it's potentially because they are fat that their thyroid potentially ain't working as it should! (Clearly there are genuine Thyroid conditions which cannot be ignored, however these are the exceptions that make the rules, the basic vicious circle principle is correct.)

So the bigger the thermogenic reaction you have the harder the thyroid works?

Nice posts guys!

Rab wrote:LOL^^^

Also....low fat, moderate carb, high protein diets are no good for dieting.

lol thats how I diet, went a bit too hard this week and lost 5lbs.

Craig wrote:

Rab wrote:LOL^^^

Also....low fat, moderate carb, high protein diets are no good for dieting.

lol thats how I diet, went a bit too hard this week and lost 5lbs.

5lb aint that much though if you lose a bit of fat, bit of water, bit of gut content and do a big shit n piss before weigh in

Thats how all these old fatties on here like GP is realising that they dont just have 10 or 12lb to lose

Am not sure that being in a proinflammatory state is primarily the result of a carb diet and plasma insulin... more a result of disproportionate levels of omega 6 to omega 3 (high omega 6, low omega 3) and disproportionately high levels of saturated fats to monounsaturated fats than it is due to insulin and blood glucose as a main factor if you ask me. All three factors are important and work together, but you can be on a very high carb diet but if your carbs are mostly low Insulin Index/high fibre foods, whole body inflammation will be pretty low... with high sat fats and omega 6's though it will always be high.

Oxidative stress from exercise and the resulting increase in ROS increases inflammation too, and in diet transfats are the worst culprit of all. Alcohol and smoking also dramatically increase inflammation by altering lipid transport into and out of the arterial cell membranes.

In respect of how to cut and carb content, there really are many ways. I mentioned gall bladders and fat digestion a few posts above - well my girlfriend had her gallbladder removed as part of a surgery about a year ago and so the way she eats HAS to be relatively high carb/protein and low fat... she's been cutting recently and in the last six weeks (following the 'train very hard/moderate calorie reduction' approach) and has gone from 20% bodyfat to 14%. The only fats her body can easily absorb are MCTs, SCTs and traces of EFAs and, problems with messed up surgeries aside, since being forced onto this kind of macro split her general health has only improved. Diet is ninety percent clean, but no guilt about a few treats either.

Interesting.

My take on it was that it was excluding good complex carbs and just a very generic "modern" diet. Which unfortunately seems to include a lot of refined carbs - pushing the inflammatory state up, and making the body have a propensity towards being in that state, rather than helping improve insulin responses and sensitivity.

Good thread, interesting posts. The most prevalent myths i see that gets me is the whole LDL cholesterol is bad, high total fat and saturated fat diets raise LDL cholesterol, therefore fat and saturated fat is bad. Unfortunately it's certainly not as clear cut as LDL cholesterol being bad, there are many subtypes of LDL molecules all differing in their atherogenic potency. T

here are two general subtype patterns, pattern A and pattern B. Pattern A is defined by a total plasma LDL subtype distribution predominantly made up of large buoyant cholesterol molecules, that cannot invade the endothelial intima because of there size and bouyancy and as a result they are at worst benign. Pattern B on the other hand consists predominantly of small dense LDL molecules that are potently atherogenic. Reducing small dense LDL cholesterol is significantly correlated with a reduction in atherosclerosis. Guess what promotes a pattern A LDL cholesterol subtype distribution? high fat diets, specifically high in saturated fat.

Not to say that it's a good idea to start chugging double cream and coconut oil, but it certainly isn't a good idea to avoid saturated fat completely. And if your worried about having high LDL cholesterol levels, then get yourself a subtype distribution test, if you are pattern A dominant then don't worry about it and continue eating the way you do and put down the statin. If your pattern B dominant then a change of diet and cholesterol lowering medication is probably a good idea.

RoB wrote:Good thread, interesting posts. The most prevalent myths i see that gets me is the whole LDL cholesterol is bad, high total fat and saturated fat diets raise LDL cholesterol, therefore fat and saturated fat is bad. Unfortunately it's certainly not as clear cut as LDL cholesterol being bad, there are many subtypes of LDL molecules all differing in their atherogenic potency. T

here are two general subtype patterns, pattern A and pattern B. Pattern A is defined by a total plasma LDL subtype distribution predominantly made up of large buoyant cholesterol molecules, that cannot invade the endothelial intima because of there size and bouyancy and as a result they are at worst benign. Pattern B on the other hand consists predominantly of small dense LDL molecules that are potently atherogenic. Reducing small dense LDL cholesterol is significantly correlated with a reduction in atherosclerosis. Guess what promotes a pattern A LDL cholesterol subtype distribution? high fat diets, specifically high in saturated fat.

Not to say that it's a good idea to start chugging double cream and coconut oil, but it certainly isn't a good idea to avoid saturated fat completely. And if your worried about having high LDL cholesterol levels, then get yourself a subtype distribution test, if you are pattern A dominant then don't worry about it and continue eating the way you do and put down the statin. If your pattern B dominant then a change of diet and cholesterol lowering medication is probably a good idea.

What do you consider a high sfa diet to be - My own high fat diet contains approx 40% of fat calories as sfa, bloodwork is spotless!

RoB wrote:Good thread, interesting posts. The most prevalent myths i see that gets me is the whole LDL cholesterol is bad, high total fat and saturated fat diets raise LDL cholesterol, therefore fat and saturated fat is bad. Unfortunately it's certainly not as clear cut as LDL cholesterol being bad, there are many subtypes of LDL molecules all differing in their atherogenic potency. T

here are two general subtype patterns, pattern A and pattern B. Pattern A is defined by a total plasma LDL subtype distribution predominantly made up of large buoyant cholesterol molecules, that cannot invade the endothelial intima because of there size and bouyancy and as a result they are at worst benign. Pattern B on the other hand consists predominantly of small dense LDL molecules that are potently atherogenic. Reducing small dense LDL cholesterol is significantly correlated with a reduction in atherosclerosis. Guess what promotes a pattern A LDL cholesterol subtype distribution? high fat diets, specifically high in saturated fat.

Not to say that it's a good idea to start chugging double cream and coconut oil, but it certainly isn't a good idea to avoid saturated fat completely. And if your worried about having high LDL cholesterol levels, then get yourself a subtype distribution test, if you are pattern A dominant then don't worry about it and continue eating the way you do and put down the statin. If your pattern B dominant then a change of diet and cholesterol lowering medication is probably a good idea.

Rob, have you looked at the interaction between LDL particle size and ApoE/apolipoprotein genotype?

I lost my hard drive contents so don't have the studies to check back on and post any more so gotta go from memory, but there are a few good trials that demonstrate fairly strongly that ApoE genotype strongly modifies any effect diet may otherwise have on cholesterol particle size (and is a stronger influence than diet)... IIRC, diets of over 50% carb content start to show physiologically significant reductions in LDL size in most but not all of the ApoE variants, while high SAT and MUFA diets raise particle size in most (but not all) groups... however, in at least one of the subgroups the SAT diet actually lowers particle sizes, and in several groups even where it raises particle size there is also a significant corrleated raise in LDL oxidation/free radical formation from the SAT diet.

From what i recall, a high fat diet predominantly based around MUFAs rather than SAT fats shows the best overall response to cholesterol size both generally and in some of the more 'at risk' genotypes of ApoE when you factor in oxidation and other issues.

ApoE genotype also has some strong correlations to blood sugar management disorders like diabetes and alzheimers, and could well be a better indicator of CVD risk than lipoprotein particle size on its own. I don't actually believe that any one factor in isolation is enough of an indicator for risk - is definitely about interactions between different factors IMO.