Why Fat Doesnt Make You Fat..

[MJ.23]

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This is brilliant, I hate the whole low fat marketing ********. The NHS don't do enough to explain this to the overweight nation. This poster explains it in laymans terms for them! Of course if only they would get of their fat arses and do some exercise that would help too!

The problem with this is that you are shifting someone from one polar opposite to the other. This will not clarify much for a lot of people and just confuse them further. It is neurile propaganda from both sides of the nutritional field which keeps people in a state of confusion. Each side constantly tries to preach their particular macronutrient and derogate the other one.

[chill9]

I agree, but it does give them some information. What I am saying is I don't think the NHS does enough to inform people of what a healthy diet entains. They should also dispel myths like 'fat makes you fat'.

[NU_nutrition_TS]

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So to burn fat we would have to burn off the food immediatley digested first?

Or all the glucose available to us our blood stream and glycogen stored in our muscles at the time?

Not quite. The body doesn't work in quite so orderly or limited a fashion.

Let's tackle each energy substrate separately.

Glucose can come from three sources:

• Directly from the food we digest (most carbohydrates rapidly break down into glucose)
• Indirectly from the breakdown - and conversion back into glucose - of glycogen stored in the liver (excess glucose from previous meals is converted to glycogen)
• From the synthesis of glucose from other substrates (e.g., glucogenic amino acids) in the liver via the process gluconeogenesis

Starting with the glucose from food. Once the glucose is in the blood stream, the pancreas will release insulin. Insulin helps partition this glucose where required:

• Directly into cells via the translocation of GLUT4 receptors so that it can be used to provide energy
• Into the liver, where it is converted into glycogen for later release
• Into adipocytes where it can be converted to fatty acids and stored as triglyceride

Storage into liver glycogen will depend on how much glucose is available (the remainder not immediately utilised for cellular energy) and how much glycogen storage capacity remains in the liver. Likewise, conversion into, and storage as, fat will depend on how much is not used immediately for energy production or stored as liver glycogen.

Needless to say, while glucose is being delivered to cells to be used to provide energy, those cells will not be using fatty acids.

When there are large amounts of glucose to be disposed of in the blood, the high level of insulin that is released blunts lipolysis to make sure that all available glucose is disposed of first before any fatty acids are released.

Fatty acids:

• Directly from foods digested
• Indirectly from the breakdown (lipolysis) of triglycerides stored in adipose tissue (from earlier dietary sources of fat or any excess glucose that was converted to triglyceride)

Since, in the average diet, most meals will contain a mixture of all three macronutrients and carbohydrates may be the major percentage of that meal, dietary fats are more likely to be stored in adipose tissue while the glucose is first disposed of in any one or more of the ways listed above.

Once blood glucose levels return to normal and insulin concentrations decrease, fatty acids can be released from storage to supply cells with energy. During this period, both fatty acids and glucose (including from the breakdown of liver glycogen or from the process of gluconeogenesis) can provide energy to cells depending on the type of cell and the demands placed upon it. For example, muscle cells will happily oxidise fatty acids at very low levels of exertion but will gradually switch to a greater and greater input from glucose (some of this may come from muscle glycogen which can supply muscle cells but cannot be released into the general circulation to supply any other cells, unlike liver glycogen).

Some cells (like red blood cells, some cells of the kidney and around 25% of the brain cells) can only use glucose to supply energy while most of the others will happily use either glucose or fatty acids (and even ketones) depending on availability or demand.

From all of the above you can deduce that, in the presence of a large amount of glucose in the blood, if energy requirements are low (sedentary/inactive) and liver/muscle glycogen stores are full then there is only fat storage left to get rid of the excess glucose. Also any fatty acids that may be present after a meal also containing dietary fats will also have to go straight into storage. However, all of these stored substrates should be able to be readily released when no food is being eaten and cellular energy demands pick up or we suddenly become more physically active.

However, if insulin levels do not readily or quickly fall to basal levels after a meal, we may find fatty acids are not optimally released from adipose tissue to provide energy to the cells. When this happens, we will probably use glucose (from stored liver glycogen or manufactured from amino acids from broken down proteins) to make up for the lack of available fatty acids. When these sources of glucose run out, we may then get hungry so that we will eat more (even though those fatty acids are still locked up and unavailable in our adipose tissue) to provide more energy to the cells. Often, because we have been relying on glucose, that hunger will manifest as a craving for more carbohydrates and the vicious cycle perpetuates and intensifies.

[NU_nutrition_TS]

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The problem with this is that you are shifting someone from one polar opposite to the other. This will not clarify much for a lot of people and just confuse them further. It is peurile propaganda from both sides of the nutritional field which keeps people in a state of confusion. Each side constantly tries to preach their particular macronutrient and derogate the other one.

To quote Randy Quaid in Independence Day: "Pay-back is a bitch!"

Obviously earlier obesity researchers felt there was a scapegoat to be had. After 'excessive calories', dietary fat became the main whipping boy (because fat has almost twice the calories of the other two macronutrients, not to mention it causes heart disease and so on).

Now that that theory is crumbling into dust, another scapegoat has to be found - if the original member of the 'gang of three' has been declared innocent, then a simple process of elimination dictates that one of the remaining two must be guilty!

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I agree, but it does give them some information. What I am saying is I don't think the NHS does enough to inform people of what a healthy diet entails. They should also dispel myths like 'fat makes you fat'.

That is the problem - the masses don't want vague conjecture and subtle nuances - they want a simple, clear-cut answer. Sometimes you have to be as one-dimensional in your presentation (as were those who blamed fat) in order to get anyone to listen to your argument!

[badly_dubbed]

Which is why fat people get hungry (and fatter) even though they have masses of stored energy?

[NU_nutrition_TS]

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Which is why fat people get hungry (and fatter) even though they have masses of stored energy?

That is the crux of the argument as presented by Gary Taubes et al. There is a 'critical mass' effect of metabolic/hormonal dysregulation where all you are doing is feeding fat storage rather than cellular energy demands. It is the inability to access your fat stores properly that leads to over-eating and continued fat accrual.

[NU_nutrition_TS]

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... a process that is only a half-truth baked up by a bunch of narrow-minded dogmatic zealots, conveniently ignoring a whole host of other factors that dont sit happy with low carbers like deteriorated mood, mental function, physical performance, blood profile, high blood glucose,impaired insulin sensitivity, etc.

I would like to close by addressing some of the other concerns raised by HTTK (see edited quote above). I will take them one at a time...

Deteriorated mood
I am assuming this may be from personal observation - certainly it is a subjective evaluation. I personally found, once I got over the difficult adaptation period, the exact opposite - an improvement in, rather than a deterioration of, mood.

Of course 'mood' is quite a nebulous concept to define but I would say, in my case, I felt calmer, less stressed, less prone to 'the blues', more positive in outlook, etc.

Since it is very difficult to measure 'mood' in a totally objective manner, you can only really find anecdotal evidence for this. Even in scientific studies, where 'measurement of mood' involves asking subjects to rate their current state by reference to a numbered scale (i.e., 1=very dissatisfied > 10=very satisfied), it is still a largely subjective process.

I think most people, irrespective of their diet, will find that their perceptions of their mood fluctuate from good/bad and can be influenced by any number of confounding variables that crop up unexpectedly and sporadically in their day-to-day lives. So I personally find this the least interesting or useful 'data' to come out of these studies.

Mental function
This, at least, can be measured in a more objective way than mood. Often the tests involved look primarily at 'cognition'. Cognition is defined as 'the mental action or process of acquiring knowledge and understanding through thought, experience, and the senses'. However, as above, many studies measure this at eight weeks. A low carb diet that initially cuts carbs drastically, such as the Atkins' Induction Phase, claim that adaptation should occur in around two weeks. Assuming this to be universally true then, if carbs are not cut as drastically, you could argue adaptation will not occur fully until much later. In which case, eight weeks may not be long enough. Alternatively, the universality of the 'two week' adaptation process, for a drastically carbohydrate-reduced diet, may be in error.

Either way, from personal experience, I would say my cognition is much better on a low-carb, high fat diet.

Physical performance
Again, I have to assume that HTTK is speaking from personal experience. As someone who does no specific training or exercise, I cannot confirm or refute that from experience. However, there is anecdotal evidence from others who eat a low carb, high fat diet and do various forms of exercise or are involved in various sports but observe no such diminution in their performance - sometimes the opposite. I dare say that high intensity activities, like resistance training, may be more prone to reduction in performance on such a diet but that may also be an individual reaction.

Blood profile
Now we get to factors that can be more objectively measured. I am assuming here that HTTK is referring to a blood lipid profile. Many people are still resistant to letting go of the lipid hypothesis, which states that high total serum cholesterol and particularly high total serum LDL cholesterol levels are risk factors for heart disease, and this often informs their opinion on the effects of a low carb, high fat diet on these parameters.

I think the tide has pretty much turned on the lipid hypothesis and though the mainstream still cling to it when issuing health and dietary advice, many researchers have shown that these parameters have little, if any, predictive quality in the aetiology of heart disease or any other condition. In fact, some would go as far as to say lower levels of cholesterol are more indicative or predictive of disease - including many associated with mood and mental disorders!

Basically some people find that total, LDL and HDL cholesterol measurements increase on low carb, high fat diet. The latter is an important observation to point out for those who still believe in the lipid hypothesis; HDL-cholesterol is supposed to be protective!

Also, what simple measures like this do not show is the type of LDL particle. Any study - or individual on such a diet - that has these LDL sub-fractions analysed, will show that the increase in LDL-cholesterol (that's the actual amount of cholesterol that is carried in the LDL particle) is due to the particles shifting from the small-dense pattern (B) to the large-fluffy pattern (A). If there is still any validity at all to the lipid hypothesis, then it is because a pattern B distribution is more problematic than a pattern A distribution. So low carbers have a much more beneficial distribution of LDL particles - more large-fluffy and fewer small-dense (pattern A) - than high carbers.

Finally, again, if the lipid hypothesis has any value it is in the association between raised triglyceride levels and heart disease. Virtually all studies have shown that triglyceride levels increase with increasing levels of dietary carbohydrate and decrease when dietary carbohydrates are restricted.

High blood glucose
This appears to be the least logical or defensible claim but, counter-intuitively, it can sometimes be true. I have experienced this myself - particularly taking fasting readings first thing in the morning. It is so well-documented it even has a name: 'dawn phenomenon'. It occurs in people irrespective of their diet and often resolves when readings are taken later in the day.

If anyone can find it, I posted a graph showing a rolling blood glucose analysis on myself while eating a low carb, high fat diet. It shows that blood glucose remained relatively stable - averaging 5.0 mmol/L - for a full sixteen hour period and only rose/dipped marginally around/between meals.

Impaired insulin sensitivity
This is the least defensible claim. I think it is based on a misunderstanding of the difference between physiological changes and pathological changes in insulin sensitivity.

Palmitic acid, a major constituent of most saturated dietary fats, tends to reduce the insulin sensitivity of muscle tissue for a transitory period. This is beneficial when consuming fewer dietary sources of carbohydrates because it allows glucose to be preferentially shuttled to cells that cannot survive without it while muscle cells use the fatty acids.

Since cells use energy substrates according to both availability as well as energy-production demands, it is a stretch to conclude that muscles will starve for glucose because of this - they will just use it (and fatty acids and ketones) more efficiently when the demand arises.

Most studies show that, overall, people who stick to a low carb diet (especially if high in fat) enjoy better lipid profiles, blood glucose levels and insulin sensitivity.

I hope debunking those half-baked 'truths' does not make me a 'narrow-minded dogmatic zealot'

[SirJinks]

Whilst I love reading threads such as these I won't profess to really understanding them completely so I'll need to ask -

Does such theory already expressed here support or contrast with the idea of carb cycling as proposed by Leangains?

[badly_dubbed]

Support, well they are very similar kind of I'd say lean gains was a modified TKD

[lev arris]

Just to stick my oar in.

I think the reason "carbs are making you fat" etc. is because companies can get away with promoting high-carb, highly-processed foods as being healthy. In honesty if the NHS proclaimed that carbs were terrible all that would happen in my mind is that the big corporates would roll-out delicious high fat, high calorie, highly processed low-carb meals. These would just replace what we have already.

In London at the weekend I needed to grab a quick meal and was really impressed that some of the "fast-food" outlets now state calories.

The way in my humble opinion to beat obesity is to print calories boldly on all food, you could then expand this to macro-nutrients. This way if people over-eat they know they are doing it.