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Today I received an email from thepaleodiet.com. I asked if they thought that most of the problems of modern civilization were a result of carbohydrates rather than saturated fats. This was their explanation.

Hi Dan,

I went to your website – congratulations on your progress.

You will no doubt lose weight on an Atkins type diet.  However, you are
missing critical micronutrients by avoiding vegetables.  Also, vegetables
and fruits are essential to maintain acid/base balance.  We spoke about this
in a recent newsletter.  So while I suspect you will get some results, I
would caution you that that approach may not be the best for optimum health
long-term.  

We do recommend olive oil as a good fat because it is high in
mono-unsaturated fats.  Ideal fat would be bone marrow, as this is the fat
that was a part of the diet of our Paleolithic ancestors.  Olive and canola
oils are simply convenient substitutes, and are much better than other
vegetable oils which are high in oomega-6 fatty acids, and low in omega-3
and mono.

Modern diseases such as metabolic syndrome are more the result of high
glycemic carbohydrate intake than saturated fat intake.  However, we are not
really genetically adapted to eat high amounts of saturated fats.  Wild
animals are very lean, and have lower levels of saturated fat than their
farm-raised counterparts.  Saturated fat affects cholesterol transport, gene
activation, and much more.  If you are interested in optimum health, we do
not recommend a diet high in saturated fats.

We may put together some more information on this topic, because there is a
lot of misunderstanding.

Best regards,

Wiley Long
Business Director
Paleo Diet Enterprises, LLC

With that said and my huge cravings for vegetables I must go back to darwinstable. To be truthful I am not really missing dairy as much as I thought I would but I DO miss the vegetables. But because I have learn’t that carbs were making me hungry I am going to keep carbs to beneath 100g a day, which seemed to be the level that I did not feel too hungry. If I am ok with that and the hunger is not too bad then I will raise my carb intake by 5g a week. Also if I am hungry then I will lower my carb intake. I am sorry for jumping around but I needed to try out atkins. It is working but I think mainly to do with low carbs, which I can still have on Paleo. Also this changes nothing about the science I was presenting earlier as this was targeting carbs and the Paleodiet is low carbs as long as you don’t gorge on fruit and starchy vegetables too much. I guess this is what this blog was all about progress.

High energy

Today I woke up with a lot of energy and my mood was really positive. This is my second day of not feeling very nauseous and so I seem to be adjusting. The other thing I have noticed is that my nails have suddenly grown really white and are much stronger rather than been all brittle. Also I am no longer using my asthma inhaler. So lots of these things make me happy. I found I was just not hungry during the day. But I have felt very minor cravings tonight but totally manageable. But it is always scary to feel those cravings because I worry that they will get worse. I know I should just eat more but I am still set in that calories matter mindset. 

My exercise routine is going strong. I noticed that I was a lot more consistent today. Usually when I exercise I start off with a bang and my heart rate stays quite low and so I have to keep turning up the levels on the treadmill then after 10mins I get tired and I slow down. But today although I didn’t get to the high levels I just cruised for 20 mins and still burn’t off the same amount of calories. So it seems that my heart rate is no longer fluctuating and is remaining a lot more stable. 

I find I am eating a LOT of eggs. But the thing is they are just so cheap and they make the most efficient low carb snack I can find or think of. I should really buy a few chickens and save myself some money:)

What I ate today:

Breakfast:

Ham salad: Ham, lettuce, chopped tomatoes, cheese

Brunch:

2 fried eggs

Lunch:

Lamb in a cucumber and yoghurt sauce: Lamb, grated cucumber, full cream yoghurt, mint

Dinner:

Steak and eggs: 2 Steaks, 1 egg, butter and garlic sauce

Supper:

3 boiled eggs

Exercise:

20 mins brisk walking (153 calories)

Total Calories:

2207 calories

20.7g carbohydrates (11.7g sugar)

168g fat (73.5g saturated fats)

179g protein

The current theory that dominates medicine, science, media and most peoples opinions today is that overconsumption of calories causes obesity. If you overeat you get fat. Simple physics right? I propose that instead of this old premise, overeating is a consequence of our body putting on fat. This is a subtle but rather major difference. If some other factor is the cause of obesity then it will make no difference how much energy we consume because this is the resulting behaviour, not the cause. I am going to try and show evidence that obesity is caused by a defect in fat metabolism and homeostasis. The human body has many biological controls on how fat is stored and any change in these controls can have large consequences that results in obesity. 

 If overeating was the cause of obesity then by reducing the calories you eat you would lose weight. This of course is obvious to everyone. But what if it is wrong? It is well known, much to the medical communities frustration, that only 1% of diets work. Clearly, reducing calories has not resulted in a reduction in obesity. In fact, in many situations obese people have been shown to consume less or as much calories as their lean counterparts but still remain obese. A reduction in calories does not necessarily mean a reduction in weight. Only on extremely restrictive diets do obese people lose weight but they are found to lose muscle and fat from their organs and often still maintain a very high level of fat in their adipose tissue – they are simply emaciated fat people. 

However, some of the best examples to prove this point is through animal studies, which can directly test whether obesity is caused by eating too many calories. We simply ask ‘when animals become obese do they do this by eating more calories’? The examples I will give involve influences from genetics, neurobiology, hormones and natural circadian ryhthm’s.  

The first example I give looks at animal hibernation, which decouples food intake from weight gain. Hibernating squirrels will double their body weight during late summer in preparation for the hibernation in winter. This is remarkably controlled and unaffected by food intake. Squirrels in the laboratory will gain this weight even if calories are severely restricted. In addition, if the fat stores are surgically removed they will still gain that fat back very quickly despite limits on calories. This seasonal fat deposition is strongly genetically programmed and is robust to changes in food supplies. 

Investigators who have looked at weight regulation and reproduction have also shown this. Female rats who have had their ovaries surgically removed exhibit a reduction in the amount of the female sex hormone estrogen. Without estrogen the rats develop out of control appetites, severely reduce their physical activity, and quickly grow obese. Rats put on weight even if their diets are restricted to what they were eating before the surgery. When estrogen is infused back into the rats they lose the weight and adopt the normal eating and exercise behaviours exhibited prior to surgery.  Thus, calorie intake and physical activity were directly influenced by a change in hormone levels.  

Mice who have had lesions applied to their hypothalamus (a region of the brain that regulates fat metabolism) become severely obese and gain six times as much weight per calorie of food compared with normal mice. These mice became so lethargic that they barely move and develop voracious appetites. Again a change in the biological controls of fat storage results in changes in eating and physical behaviour – not the other way round.  

Genetic studies on obese strains of rats show that individuals that are placed on a restricted diet from birth onward, grow fatter by adulthood than their littermates who were allowed free reign over what they ate. Therefore, calories did not effect the obesity of these rats over their lifetime. Quite the reverse a reduction in calorie consumption seemed to be associated with increased obesity.  In addition, those rats on a restricted diet had 50% less muscle mass than normal rats and 30% less muscle mass than their counterparts who could eat what they wanted. Emaciated fat mice. 

It is clear from these animal studies that the intake of calories has no influence on weight gain. In some cases the animals would severely reduce their physical activity becoming very lethargic. However, it would be difficult to propose that a reduction in physical activity was the CAUSE for these changes but rather an associated behaviour. These studies certainly suggest that the cause of obesity is some error in fat metabolism or homeostasis that leads to increases in fat deposition and changes in behaviour (overeating, lethargy). 

In this final and human example I hope to put an end to the hypothesis that overeating is the cause of obesity. There is a rare condition known as lipodystrophy. In one case in 1913, a ten year old girl first loss fat from her face, then, over the next three years, this emaciation gradually extended down her trunk and arms. Obesity of the lower body began at fifteen and by the time she was 24 she had all the body fat localised in her lower waist. You can see the example below. 

This is clearly not a case of overeating. The most obvious explanation is fat was placed due to some genetic or hormonal condition. In fact, this is seen in the differences between the sexes. Males tend to store fat around the waist while females at the hips and this is large genetically and hormonally controlled. Although these are obvious examples they do beg the question – is fat deposition controlled by our biology and physiology or is it controlled by our behaviour. If it is not controlled by our behaviour then it is difficult to argue that obese humans are that way because they have no willpower, eat too much and do not exercise. Obesity is likely to be a defect in fat metabolism which results in overeating and lethargy. Asking obese people to change their eating patterns or to exercise more is equivalent to telling a seven foot man that they need to stop eating and exercise less in order to become shorter. 

Soon, I will talk about how I think obesity is controlled by our biology, how we get fat DESPITE calorie consumption and what we can do about it.

Satiated

I cannot believe that I only ate 1600 calories today and I am NOT hungry. I simply am amazed at this. I literally do not feel hungry at all. I am starting to get used to the meals and that horrible nausea has gone. But most of all I am simply NOT hungry. Still feeling a little weird about not eating the veges but I did have a whole brocolli head today and it didn’t blow me over my carb budget. So I think I am getting to know how to do this. 

On a more negative note I didn’t do so well on the exercise today. My heartbeat was rising very quickly and I did not burn off as much calories as I normally do by keeping my HR between 145-155 heartbeats per minute. I will monitor this. 

Today I ate:

Breakfast:

50g Edam Cheese

Lunch:

Curry Chicken: Full cream yoghurt, Garam Masala, Turmeric, Cloves, Garlic, Chilli, Ginger, Brocolli, Skinless Chicken, Mint, Canola Oil

Dinner (ATKINS STYLE)

Pork, Eggs & Butter

Exercise

20 Mins Brisk Walking on Treadmill – 143 calories

Total Calories – 1623

Carbohydrates – 20g (13.6g sugar)

Fat – 90g (33.1g Saturated Fat)

Protein – 206.7g

Huge weight loss

WOW. Since monday (it is now wednesday) I have lost nearly 2 kilograms or 4.4 pounds. Basically ever since I severely reduced my carb intake on Atkins this has been happening. It is amazing!!! My hunger levels have bottomed out to be sure. I feel a little bit ‘arrggghhh’ at eating meat, eggs and cheese all the time with little veges or fruits. But I am soldiering on as I know the veges will return and I will be a happy camper. For now I will keep drinking water to feel refreshed. 

Yesterday I ate:

Breakfast:

Glass of Milk

Lunch:

Minced beef, tomato slice, edam cheese, 5 onion rings

Afternoon Snack:

Steak, olive oil, garlic

Dinner:

Steak (more), lettuce, tomato slice, 5 onion rings, edam cheese, fried egg

Exercise:

20 mins brisk walking – 154 calories

Total Calories – 1931

Carbohydrates – 19.2g (15.3g sugars)

Fats – 125.1g (51.1g saturated)

Protein – 207.4g

A new Oxford led university study has shown that the greater the levels of Insulin-like Growth Factor-1 (IGF-1) the greater the chances of developing prostrate cancer. Researchers looked at the data of blood samples of 3700 men with prostrate cancer and 5200 men without it, and found higher levels of IFG-1 in the cancer group. Dr Lesley Walker from Cancer Research UK stated ‘there are no clear data on modifiable risk factors’ and also suggests that this work could be helpful in developing drugs (I assume to lower IGF-1 in the blood stream). 

The theory behind IGF promoting cancer goes like this. Cells get energy by binding IGF-1 to the cells IGF-1 receptors, and this causes available glucose in the bloodstream to be directed to that cell. This glucose is the main energy source of cells. Cancer cells have been shown, compared to normal cells, to have an extremely large number of IGF-1 receptors on their surface, thus gaining far more energy or glucose in order to promote growth. This is because cancer cells grow by ‘fermentation’ or anaerobically and thus require far more energy than normal aerobic cells. It has been shown that when tumors are transplanted into mice that have been genetically engineered not to produce IGF-1 the tumor growth is retarded if not eliminated altogether. Effectively the cancer cells are starved of energy (glucose) that is needed for growth and division. If IGF is then injected into the mice the tumors begin to grow. Thus it seems that IGF-1 is vitally important in providing the large amounts of energy that the cancer cells require. 

In the bloodstream, virtually all insulin-like growth factors are attached to small proteins (binding proteins) that carry them around the blood vessels.  When attached to these binding proteins the IGF’s are too large to pass through the walls of the blood vessels in order to get to the cells where the IGF can be used. At any moment, only a small percentage of IGF is left unbound in the circulation to stimulate the growth of cells (including cancer cells). These binding proteins are another mechanism that the body uses to regulate hormonal signals and growth factors. However, insulin depresses the concentration of these IGF-binding proteins. So after a large carbohydrate meal, plenty of glucose enters into your bloodstream causing insulin levels to rise and results in these binding proteins been taken out of circulation. As a consequence, this increases the amount of unbound IGF that can then go and supply potential cancer cells with much needed energy.  

Perhaps one of the ‘risk factors’ that should be mentioned is diets that are high in carbohydrates, result in elevated levels of insulin, which can then, through its various control mechanisms, promote cancer growth. This may help explain why in diabetics there is a much higher chance of developing cancer. Higher insulin levels result in more unbound IGF which can then go and feed cancer cells. Surly, this would be worth mentioning when you consider that in the UK, where this study is done, prostrate cancer is the second highest cancer to kill men.