The Brown Fat Revolution

Ok so you now understand that according to “The Brown Fat Revolution”, this fat is your friend, and you need it for a younger-looking, slim, toned body. It’s the white fat in our bodies that makes us flabby and age poorly primarily because white fat is an “inflammatory” storage “organ” which prematurely ages our systems.

Complication of the overweight/ obese state exacerbate with age and tends to carry a poor prognosis.  Brown fat, on the other hand, boosts your basal metabolic rate, keeping you slim and giving skin volume a better appearance. Brown fat may actually help you lose weight by thermogenically increasing basal metabolic rates. The Brown Fat Revolution is not so much a weight loss diet as an eating and exercise plan designed to help you increase metabolism, get rid of white fat, and replace it with healthy brown fat.

I have spent years as an exercise cardiologist studying and assessing people of all shapes and size and have seen how diet manipulation and exercise can change your visceral fat, rejuvenate your appearance, and enhance weight loss and more importantly improve quality-of-life and reduce cardiovascular morbidity and mortality.

Essentially coupling a keto-adapted diet (“Eco-Atkins”) with daily conditioning exercise you will maintain ketosis and stimulate and activate brown fat.

Stick to the 60:30:10 philosophy I have described with 60% of daily calories from fat (balance lean red/ white meat, oily fish, eggs, low fat dairy and some cheese with the vegan oils and fats). 40% of calories from protein to 1-1 1/2 grams per kg body mass (do not overdo the protein). The 10% calories come from your carbohydrate restriction (about a total 60g per day only).  This for me is the BIGGEST challenge as it is terribly easy to intake carbohydrates.  Keep away from the big 5 (potatoes, rice, pasta, bread and pizza), all cereals, starchy vegetables, high-carb fruits and ALL fruit juices cakes cookies, sweets and sugars.

Use the glycemic index to choose the best carbs — high-fiber ones like occasional fresh fruits, vegetables and legumes. Don’t forget raw nuts and seeds are vital for vegan fat calories, great protein and high in fibre (this will deal with constipation). Eat before and after every workout and keep total calories proportional to your goals (20 calories per kg if aiming for weight loss) to 30 calories per kg if aiming to retain a lean mass with good muscle bulk. Eat a variety of foods throughout the day in small volumes keeping portions small and drink plenty of ‘calorie free’ fluids.

In my next series of BLOGS I will discuss “Optimal Medical Management” (OMT) in preventing and aggressively treating cardiovascular disease.

Blessings

Cardiologydoc

 

Brown Fat and Obesity

Obesity results from an imbalance between energy intake and expenditure.  The adipose-tissue pool in mammals is composed of at least two functionally different types of fat: white and brown. White adipose tissue is the primary site of energy storage and of release of hormones and inflammatory cytokines that modulate whole-body metabolism and insulin resistance.  Excess accumulation of white adipose tissue is the prime cause of obesity.

Brown adipose tissue, on the other hand, is important for both basal and inducible energy expenditure in the form of thermogenesis (heat generation) mediated by the expression of the tissue-specific uncoupling protein 1 (UCP1).

Brown adipose tissue affects whole-body metabolism and may alter insulin sensitivity and modify susceptibility to weight gain. Estimates suggest that as little as 50 g of maximally stimulated brown adipose tissue could account for up to 20% of daily energy expenditure in an adult human.

There is evidence that stimulating adaptive thermogenesis, defined as the facultative heat produced in response to cold and diet manipulation (like keto-adaptation), might serve as a means of preventing or treating obesity; thus, it is of interest to understand the mechanisms underlying adaptive thermogenesis.

Individual differences in energy expenditure can have large, long-term effects on body composition and weight. Several prospective studies have shown that a relatively low energy expenditure predicts a gain in body weight (often due to low basal metabolic rates). Hence, adaptive thermogenesis may be an attractive target for anti-obesity therapies.

Many studies have indicated that brown adipose tissue in rodents has profound effects on body weight, energy balance, and glucose metabolism, and the presence of brown adipose tissue has been observed in adult humans under circumstances of long-term exposure to cold or of hyper adrenergic stimulation in pheochromocytoma.  

Of great interest to me with my understanding of keto-diets and keto-adaptation, that certain dietary fuels such as fatty acids, and some drugs can alter expression of brown fat. Interestingly Beta-blockers are associated with weight gain in clinical practice possibly due to suppressed brown fat expression (through blocking adrenergic stimulation).

The depots of brown adipose tissue have similar distributions in both men and women, but the mass and activity of brown adipose tissue are greater in women than in men. Other factors appear to be associated with a higher mass of brown adipose tissue. There appears to be an interaction between brown adipose tissue and obesity with an inverse correlation between the prevalence of detectable brown adipose tissue and BMI (higher BMI correlates low brown fat); suggesting that higher levels of brown adipose tissue may protect against age-related obesity (remember to survival affect in neonates)..

 

These results are consistent with murine studies showing that strains with higher levels of intermuscular brown adipose tissue are protected from diet-induced obesity and diabetes. 

Humans, like mice, have a range of metabolic rates. Thus, methods to stimulate generation and activation of brown adipose tissue might lead to new approaches to promoting weight loss and increasing insulin sensitivity (as we see in keto-adaptation). There is recent evidence that brown adipose tissue is embryonically more closely related to skeletal muscle than to white adipose tissue. A putative shared lineage between brown adipose tissue and skeletal muscle may provide clues about the origins of stem cells that lead to the formation of brown fat and to adaptive thermogenesis. This also raises important questions as whether physical training can stimulate and activate brown adipose tissue, adding to maintaining a high metabolic rate.

I think you will agree we are a remarkably beautifully created people in the image of God.

1 Timothy 2:6

6 If you point these things out to the brothers and sisters, you will be a good minister of Christ Jesus, nourished on the truths of the faith and of the good teaching that you have followed. 7 Have nothing to do with godless myths and old wives’ tales; rather, train yourself to be godly. 8 For physical training is of some value, but godliness has value for all things, holding promise for both the present life and the life to come. 9 This is a trustworthy saying that deserves full acceptance. 10 That is why we labor and strive, because we have put our hope in the living God, who is the Savior of all people, and especially of those who believe.

Blessings

Cardiologydoc

Could it all be about “Brown Fat”?

Proverbs 4

Get Wisdom at Any Cost

1 Listen, my sons, to a father’s instruction; pay attention and gain understanding. 

12 When you walk, your steps will not be hampered; when you run, you will not stumble. 

23 Above all else, guard your heart, for everything you do flows from it.

 Is it all about the “Brown Fat”?

Brown adipose tissue or brown fat is one of two types of fat or adipose tissue (the other being white adipose tissue) found in mammals.

It is especially abundant in newborns and in hibernating mammals. Its primary function is to generate body heat in animals or newborns that do not shiver. In contrast to white adipocytes (fat cells), which contain a single lipid droplet, brown adipocytes contain numerous smaller droplets and a much higher number of mitochondria, which contain iron and make it brown. Brown fat also contains more capillaries than white fat, since it has a greater need for oxygen than most tissues.

Biochemistry:

The mitochondria in a cell utilize fuels (glucose or ketones) to produce energy (in the form of ATP). This process involves storing energy as a proton gradient, also known as the proton motive force (PMF), across the mitochondrial inner membrane. This energy is used to synthesise ATP when the protons flow across the membrane (down their concentration gradient) through the ATP synthase enzyme; this is known as chemiosmosis.

In warm-blooded animals, body heat is maintained by signalling the mitochondria to allow protons to run back along the gradient without producing ATP. This can occur since an alternative return route for the protons exists through an uncoupling protein in the inner membrane. This protein, known as uncoupling protein 1 (thermogenin), facilitates the return of the protons after they have been actively pumped out of the mitochondria by the electron transport chain. This alternative route for protons uncouples oxidative phosphorylation and the energy in the PMF is instead released as heat.

Brown adipose tissue is highly specialised for this non-shivering thermogenesis. First, each cell has a higher number of mitochondria compared to more typical cells. Second, these mitochondria have a higher-than-normal concentration of thermogenin in the inner membrane.

Function in infants:

In neonates (newborn infants), brown fat, which then makes up about 5% of the body mass and is located on the back, along the upper half of the spine and toward the shoulders, is of great importance to avoid lethal cold (hypothermia is a major death risk for premature neonates). Numerous factors make infants more susceptible to cold than adults:

  • The higher ratio of body surface (proportional to heat loss) to body volume (proportional to heat production)
  • The higher proportional surface area of the head
  • The low amount of musculature and the inability or reluctance to shiver
  • A lack of thermal insulation, eg., subcutaneous fat and fine body hair (especially in prematurely born children)
  • The inability to move away from cold areas, air currents or heat-draining materials
  • The inability to use additional ways of keeping warm (eg., drying their skin, putting on clothing, moving into warmer areas, or performing physical exercise)
  • The nervous system is not fully developed and does not respond quickly and/or properly to cold (eg., by contracting blood vessels in and just below the skin).

Heat production in brown fat provides a baby with an alternative means of heat regulation and is critical to our survival of our species.

Deuteronomy 7:15

The LORD will keep you free from every disease.

Presence in adults:

It was believed that after infants grow up, brown adipose tissue should not be required for survival as the adult should have the skills to manage ALL the factors above.

Recent studies using Positron Emission Tomography scanning of adult humans have shown that brown fat is however still present in very small amounts in adults in the upper chest and neck. The remaining deposits become more visible and active in slim trim adults since brown fat takes calories from normal fat and burns it with high efficiency and increases metabolic rates.

Embryology:

Brown fat cells and muscle cells both seem to be derived from the same stem cells in the embryo. Both have the same marker on their surface (Myf5, myogenic factor), which white fat cells do not have. Brown fat cells and muscle cells both come from the middle embryo layer (mesoderm), the source of myocytes (muscle cells), adipocytes, and chondrocytes (cartilage cells). Adipocytes give rise to white fat cells and brown fat cells.

 

Researchers found that both muscle and brown fat cells expressed the same muscle factor Myf5, whereas white fat cells did not. This suggested that muscle cells and brown fat cells were both derived from the same stem cell. Furthermore, muscle cells that were cultured with the transcription factor PRDM16 were converted into brown fat cells, and brown fat cells without PRDM16 were converted into muscle cells.

This common stem cell theory may be an important for stimulating and activating brown fat through actively maintaining muscle mass as we age.

In my next BLOG on this subject I will talk on the mechanisms to increase activity and expression of Brown Fat.

Blessings

Cardiologydoc

The easy option – Eco-Atkins ketogenic diet

The “Eco-Atkins modified lifestyle CAN be a solution to your weight loss woes if you’ve tried other approaches and can’t seem to achieve your goals. Another reason to try a modified version of this popular weight loss routine are the concerns about intake of high animal and saturated fats.

When you modify this ketogenic diet to include more vegan/ oily fish components and more polyunsaturated and monounsaturated fats particularly of the Omega 3 group you may not lose weight as quickly, but for me it meant I could stick to the “rules” more easily. For me this was a fair trade-off. The most important thing to keep in mind when modifying this ketogenic diet is that the key is STILL keeping everything low carb. If you can do this, you can make some minor changes and still lose weight.

The part of the Atkins plan that gave me trouble was what I had to eat to fill me up in place of the carbohydrates I cut out of my diet. I simply wasn’t able to eat a lot of meat and fatty foods like cheeses. Instead of loading up on these, I modified the typical ketogenic diet menu plan by balancing out my meals with more fish, vegetables and salad greens that are permitted on the typical Mediterranean type diet.

For instance, raw nuts and seed are an ideal source of unsaturated fats; fibre and protein but keep volumes down to ~ 100 -150 g per day.

Do NOT Substitute with Carbs.  Strictly NO potatoes; no rice; bread; pasta; pizza; chips……………….

Happy keto dieting

Cardiologydoc

Ketones – What are they?

INTRODUCTION: 

Ketones are a beneficial product of fat metabolism in the body. When the body breaks down stored fat, it creates fatty acids, which are then burned in the liver in a process called beta-oxidation. This process results in the creation of ketone bodies, which are then used as fuel by the muscles and brain cells.

 

There are three major types of ketone bodies present in the human blood stream when the metabolic process of ketosis is in progress:

 

Acetoacetate (AcAc)

Beta-hydroxybutyrate (BHB)

Acetone

In times of starvation and low insulin levels, ketone bodies supply up to 50% of the energy requirements for most body tissues, and up to 70% of the energy required by the brain. Although glucose is the main source of fuel for neurons when the diet is high in carbohydrates, these fatty acid fragments are used preferentially by brain cells when carbohydrate or food intake is low.

During fasting or low carbohydrate intake, normal levels of ketone bodies in the blood stream can rise to levels between .5mM and 5 mM, depending on the amount of protein and carbohydrates consumed.

There is some evidence for enhanced athletic (endurance type sports) performance using ketones as sole fuel.

After a few weeks of adapting to a ketogenic diet the levels of ketone bodies rise, the brain begins to use more than half of them for fuel.

In addition, the muscles of the body use all of the ketone body types. But after a few weeks of keto-adaptation, the muscles start converting the acetoacetate into beta-hydroxybutyrate (BHB) and returning it to circulation, as the brain prefers to utilize BHB for fuel.

So as time goes on, and the muscles convert more acetoacetate to BHB, the levels of beta-hydroxybutyrate ketones increase, and the acetoacetate levels decrease. This is important to know because the Ketone stix you buy in the store only test for Acetoacetate, not beta-hydroxybutyrate ketones.

 

So the longer you are eating low carb, the less MEASURABLE ketone bodies will show up on the Ketostix. In other words, it will seem like ketosis is slowing. However, at this point, your brain will be happily burning the beta-hydroxybutyrate ketones for fuel, and as long as you stay under your carb sensitivity levels, you will be burning fat for fuel (and burning the pathological visceral fat around your gut and waist).

STAYING IN KETOSIS:

For most people, taking in adequate calories (30 calories per kg body mass) and eating 1.5 grams of protein per kg per day; keeping carbohydrate reduced to ~ 50-60 g/day will keep you in ketosis provided the balance of daily calories are ingested as FAT.  Therefore 60% of daily calores per day should come from fat; 30% calories from protein and ~ 10% from carbohydrates (if you are trying to lose weight then cut daily calories by 1000-1500 calories daily).

It is important NOT to overdo the protein intake as this is TOXIC to the liver and kidneys and will also short circuit the ketosis as too much protein intake will produce glucose (via the Cori Cycle). Finally those with carbohydrate sensistivity will need to restrict daily carbohydrate to < 40 g/d to maintain ketosis.

Ultimately you have to know in detail the nutritional value of each foodstuff including the gram content of protein; fat and carbohydrate and also the total energy content of the product eaten.  For 1g of fat = 9 calories; 1g of protein = 5 calories and 1g carbohydrate = 4 calories.  Keeping daily records of exact intake; total energy; exercise and daily body mass will make your journey more interesting and productive.

Enjoy the ketones.

Cardiologydoc

Eco-Atkins Ketogenic Diet

“Eco-Atkins” plant-based, low-carbohydrate diets-might not only lower weight but also lower blood levels of LDL cholesterol and elevate HDL-C, a one-month study suggests.

The study investigated 44 overweight men and women with hyperlipidaemia who were randomised to the low-carb “eco-Atkins” diet or to a lacto-ovo vegetarian version of the DASH diet.

While individuals in both groups lost a “fairly dramatic” 4 kg, those following the “eco-Atkins” diet had a greater decrease in LDL-C. The study message is:”Use more plant foods to lower LDL-C-whether it is oils, proteins, carbohydrates, or fiber”.

 

“We conclude that low-carbohydrate diets emphasising vegetable sources of protein, such as gluten, soy, and nuts, together with vegetable oils, can be used in weight-reduction diets to improve serum lipid concentrations,” the researchers write.

The dietary dilemma is choosing the optimal proportion of fat, protein, and carbohydrate for weight loss plus cholesterol-lowering can be a dilemma.

A low-carb, high-meat diet-such as the Atkins diet-can induce weight loss, lower triglycerides, and raise HDL-C levels, but it also tends to increase LDL-C levels. On the other hand, a high-carb, low-animal-product diet lowers cardiovascular and pathological ageing risk factors.

 

To determine weight loss and the effect on serum lipid concentrations from a low-carb diet where plant sources replace animal-based proteins and fats, the researchers compared the “eco-Atkins” diet with a control diet.

The “eco-Atkins” diet replaces meat, eggs, and butter with plant-based nutrients, which makes it more ecologically friendly in terms of the use of land resources and the cost of agriculture.

This test diet provided the minimum level of carbs recommended by the National Academy of Sciences Institute of Medicine-130 g/day-by eliminating starch-based bread, rice, and potatoes but including high-fiber oat-bran cereal and vegetables such as okra and egg plant. Protein sources included nut bread and tofu. Fats included olive oil, nuts, and avocados.

The researchers compared this with a positive control diet that would be expected to benefit heart health. The control diet extended the DASH diet in that it allowed low-fat dairy products, egg substitutes, and whole-grain products but eliminated rather than reduced meat consumption.

The researchers studied 44 overweight men and women with hyperlipidaemia. The subjects were randomised to the test diet-27% carbohydrates, 30% protein, and 43% fat-or control diet-58% carbohydrates, 17% protein, and 25% fat. All diets were designed to provide 60% of estimated calorie requirements. Prepared diet foods were shipped to the subjects.

Weight loss was similar in both groups. However, those in the low-carb, plant-based diet group had greater reductions in LDL-C levels and in the ratio of total cholesterol to HDL-C. They also had more beneficial changes in apolipoprotein levels and small but significantly greater changes in blood pressure.

Ageing and Nutrition (part 3) – it’s all about Insulin

To really understand the rationale and physiology of keto adaptation I will give a brief overview of the chemistry of Insulin.  I personally believe this is the villain of modern day obesity and metabolic syndrome where Insulin Resistance and hyperinsulinemia are the rule.

Insulin is a polypeptide hormone that promotes glucose utilization, protein synthesis and the formation and storage of lipids. Produced by specialised endocrine cells of the pancreas called the islets of Langerhans, insulin was discovered in 1921 by two Canadian researchers, Dr Frederick Banting and his medical assistant Charles Best.

Insulin is crucial to the transport of glucose and amino acids into muscle cells. Properly managed by the right diet, insulin is the athlete’s best friend as it plays an enormous role in muscle hypertrophy (growth). With the support of human growth hormone (hGH), it has a direct effect on the production of somatomedins in the liver. Somatomedins are called insulin like growth factors or more commonly IGF. For this reason insulin has earned the reputation of an anabolic hormone.

However, insulin is a double-edged sword. It is also the hormone of feasting and plenty and depending on what is eaten and when, insulin functions as a brilliant fat storage hormone.

Our ability to respond to insulin is called insulin tolerance. The more tolerance a person has for insulin, the more insulin it takes to get a response (this is Insulin resistance). A low tolerance to insulin is preferable, as excessive insulin production is associated with obesity, high cholesterol, high triglycerides, hypertension, vascular disease, fatigue and adult-onset type II diabetes. Many overweight individuals have excess insulin in their blood due to excessive stimulation of the pancreas. This condition is called hyperinsulinemia.

The hallmark of the metabolic Syndrome is resistance to insulin, which many experts claim is caused by eating too many processed high-carbohydrate foods. This common dietary practice, where carbohydrates generally make up 65% of daily calories, in turn causes an excess build-up of glucose in the blood resulting in the production of free-radicals and advanced glycaemic end products (AGEs) by couple glucose the protein molecules.  AGEs causes the proteins to malfunction and is thought to be key in the pathology driving unhealthy ageing.

Metabolic Syndrome was coined in 1988 by Dr. Gerald Reaven, a Stanford University endocrinologist, and defined by a cluster of related symptoms that always includes insulin resistance and one or more of the following conditions; abnormal blood fats, elevated uric acid, reduced HDL, increased oxidized LDL particles, overweight and high blood pressure.

Insulin resistance involves the release by the pancreas of more insulin than the target cells in the body can handle. Excess carbohydrate intake in the form of sugar, bread, potatoes, pasta, bagels, chips, cookies, breakfast cereals, etc cause blood glucose levels to rise excessively, and in response, the pancreas releases more and more insulin. Eventually, the cell receptors of muscle and vital organs become saturated, non-responsive and may even shut down. Then, glucose and insulin begin to accumulate to toxic levels in the bloodstream, becoming agents of hostility and damage. Clotting factors are activated and advanced glycation end products (AGEs) begin to form. It is estimated that as many as 40% of North American adults have this syndrome.

Sleep deprivation depresses growth hormone release, slows muscle and strength gains and negatively influences immune function. Insomnia and sleep deprivation also cause insulin resistance, which promotes intra-abdominal obesity. This translates to that dreaded spare tire around the gut, which happens to be the most dangerous region to store excess bodyfat in terms of disease risk for the body, especially heart disease.

Ideally, we don’t want to constantly flood the body with high-glycemic, low fiber, low water volume carbohydrates such as sugar and white flour, as this causes insulin to spike. It’s much better to consume minimal carbohydrates that are metabolized slowly and that release their sugars over a longer period of time.

Consuming low-glycemic carbs in smaller portions keeps glucose and insulin closer to a normal fasting baseline for a good anabolic effect, not too high or too low.

Another problem with high Insulin is suppression of testosterone levels, adding to impaired muscle strength and performance and sexual dysfunction.

Nutrients that optimize insulin activity, improve its sensitivity and protect it and the pancreas from oxidative damage include B6, niacin, magnesium, chromium, vanadium, alpha-lipoic acid, vitamin C and the omega-3 fatty acids, including alpha-linolenic acid and eicosapentanoic acid (EPA) and decosahexanoic acid (DHA).

Insulin has a direct effect on the metabolism and storage of fat. For instance, insulin accelerates the transport of glucose from the blood into cells and the conversion of glucose into fatty acids. This is called lipogenesis. Insulin has a greater half-life than glucose, so any insulin left circulating in the blood after it has completed its work is also converted into fat. And the effect is even more reliable if by genetic predisposition you have a slow metabolic rate and spend most of your free or work time seated.

If levels of insulin climb too high, which can happen simply by eating a large meal or a meal dominated by carbohydrates such as bread, rice or pasta, a simultaneous increase in the enzymes lipoprotein lipase and acetyl-CoA carboxylase occurs. Both of these enzymes facilitate the transport of fatty acids into fat cells. High insulin levels activate lipoprotein lipase and increase its activity. Lipoprotein lipase promotes the removal of triglycerides from the bloodstream and encourages their deposition in adipocytes or fat cells. Insulin also inhibits the action of hormone-sensitive lipase which breaks down stored fats for use as energy. So anytime you catch yourself eyeing a muffin or a slice of bread, focus for a moment in advance of the indulgence. Think of what effect it will have on your blood chemistry and body composition. Remember, insulin inhibits the mobilisation of stored fat and promotes fat deposition add to the visceral adiposity.

If insulin levels are continuously sustained above baseline throughout the day, enzymes like lipoprotein lipase can suppress the oxidation of fatty acids, even while consuming a negative calorie intake combined with exercise. This is called an anti-lipolytic (anti-fat beakdown) effect where your fat stores are preserved even though total calorie intake may be quite low. While the caloric profile of food is a factor in weight management, the chemistry of food is more important to understand. The irony of this is that few people really get this concept or even think about it.

Blessings

Cardiologydoc