The Primal Origins of the Human Diet

The Origins of the Human Diet

Deep in the milky-way lies a wispy, barely detectable, gaseous interstellar cloud which contains an 8-atom sugar called glycolaldehyde. This chemical may just be a major precursor to life on planet Earth.

Sugar molecules in the gas surrounding a young Sun-like star

Glycolaldehyde can react with ribose, a 3-carbon sugar, to form RNA and DNA. DNA, or deoxyribonucleic acid, is like a biological blueprint that a living organism must follow to survive and remain functional. RNA, or ribonucleic acid, helps carry out this blueprint's guidelines. RNA transfers the genetic code needed for the creation of building-block-proteins from information-storing-nuclei to the protein manufacturing segments of our body’s cells.

Think of DNA as a blueprint or set of instructions. RNA contains a second set of instructions for converting the blueprint into the biological house we live in. Together, they form the basis for life on this planet. Glycolaldehyde is one of the keys to the creation of both.

The same interstellar cloud that contains glycolaldehyde also contains a sweet compound called ethylene glycol. It is a close relative of sugar. This is an important actor when looking into early life on earth. In earth’s earliest days, the atmosphere contained no oxygen. Without oxygen, life was based on the production of energy using anaerobic processes that did not require the presence of oxygen. These anaerobic processes, (requiring no oxygen), allowed for the conversion of sugars as well as early forms of protein into energy. However, another kind of process was needed for fats. This requirement for a second process is a key concept in understanding how our metabolisms work at their most basic level.

The first living cells were prokaryotic in nature. Prokaryotic cells are microscopic single-celled organisms that have neither a distinct information rich nucleus with a membrane nor any other specialized oxygen-based sub-structures. Understandable since in earliest times there was no oxygen present. This means that all of the living cells on the planet were identical in their genetic structure. It also means that they primarily metabolized sugar for energy. However, there was a very important side effect to this process!

The oxygen that fills our atmosphere today was built up over millions of years as a waste-product from the prokaryotic cells' anaerobic digestion of sugar. Once there was enough oxygen to go around, prokaryotic cells evolved into eukaryotic cells and almost all the life we see each day — including all plants and animals, are Eukaryota. Eukaryotic cells are far more complex and diverse than prokaryotes. They contain a nucleus, which stores a unique genetic blueprint. Eukaryotic cells also boast their own personal "power plants", called mitochondria. They thrive in an oxygen rich environment. These tiny cellular substructures produce chemical energy and they hold the key to understanding the evolution of life on earth. They ushered in a whole new era. These complex eukaryotic cells eventually evolved into multicellular organisms.

But how did the eukaryotic cell itself change into more complex life forms? How did such a simple life form make the evolutionary leap from a prokaryotic cell to a more complex eukaryotic cell to plant and animal cells? The answer to these questions is a powerful statement about life on earth. Eukaryotic cells evolved through teamwork.

Evidence supports the idea that eukaryotic cells are actually the product of separate prokaryotic cells that united together in a symbiotic union. In fact, the mitochondrion itself seems to be the "great-great-great-great-great-great-great-great-great grandchild" of a free-living bacterium that was engulfed by another cell. This bacterium ended up becoming a sort of perpetual houseguest. The host cell benefitted immensely from the chemical energy produced by the guest it was hosting (now called the mitochondrion). The mitochondrion in turn profited from the shielded, nutrient-rich environment surrounding it.

It is our mitochondria that produce energy by using oxygen to burn fat. Fat is an aerobic nutrient. It forms the very foundation of oxygen-based metabolisms. Fat cannot be used for anaerobic (non-oxygen-based) conversion to energy.

Essential Nutrients, Nonessential Excesses and Disease

We can discuss essential nutrients in two broad categories; macronutrients and micronutrients.

You are what you eat, and you eat what you are: fats, proteins and carbohydrates. You also must consume various other vitamins and minerals.  First we need to discuss macronutrients and then we will look at micronutrients.

What are macronutrients? Nutrients are substances essential for growth, metabolism, and other bodily functions. Macronutrients are nutrients that provide our bodies with the calories and building blocks required to make and use energy. “Macro” means large. Macronutrients are the nutrients needed in large amounts. They tend to be complex and composed of several substances. There are three macronutrients: fat, protein and carbohydrate.

What are micronutrients? Micronutrients are the vitamins, minerals, trace elements, phytochemicals, and antioxidants that are essential for good health. Micronutrients generally get a lot of attention because they can be packaged and bottled (for profit). However, when it comes to health and vitality it is ultimately macronutrients that run the show.

Nutrition has become a very confusing subject for discussion these days. What follows is basic description of the science behind what various macronutrients do and what our basic requirements are for their consumption. To be clear, this blog has strong reservations about the value of manufactured foods.  All foods that were not given to us by mother-nature directly and which require significant processing should be removed from daily life if your goal is health and longevity. This includes manufactured so-called health foods and commercially prepared factory farmed meats.

The category of macronutrients can be broken down into two subsections, essential and non-essential. Essential nutrients are nutrients that your body cannot manufacture for itself. Essential nutrients must come from external sources. Non-essential nutrients are nutrients that can be accessed internally or manufactured by combining a variety of other available nutrients.

There are essential micronutrients as well. These include the various B vitamins, vitamin C, and the fat soluble vitamins A, D, E & K. They must be accessed externally. There are also many essential minerals, including: Calcium, Chloride, Chromium, Cobalt (as part of Vitamin B12), Copper, Iodine, Iron, Magnesium, Manganese, Molybdenum, Phosphorus, Potassium, Selenium, Sodium, Zinc.

Note: There are no essential carbohydrates or sugars, all carbohydrates eventually become sugar. Why are there no essential carbs? Because we can make them via the synthesis of amino acids and glycerol obtained from fat metabolism. We can also make them through de novo synthesis (also called gluconeogenesis). Eventually, the body can adapt to a low-carbohydrate state by producing ketones (a state called ketosis) to fuel the body/brain. We can readily adjust to using ketones for fuel, except where excessive carbohydrate stores are present.  In that case, our bodies will revert to running on sugar.

We do not need carbohydrates. In fact excessive intake of carbohydrates is the cause of major diseases of affluence in the world today. These diseases include huge increases in rates of cancer and heart disease. Cutting excessive sugars and carbohydrates out of our diets will prevent a vast proportion of these diseases! We know this having observed the effects of fasting and caloric restriction.

Fasting and caloric restriction both reduce levels of insulin, which is required for the storage of blood sugar in the form of fat. Eating fat doesn’t make you "gain weight" directly. However, eating excessive amounts of sugar along with that fat is what causes us to pack on excessive and unhealthy pounds.

As well, fasting and caloric restriction reduce another growth factor called MTOR (short for mammalian target of rapamycin), which regulates cell growth and cell proliferation. MTOR is a protein sensing pathway that sets a limit on the amount of protein we can eat before it starts creating negative health effects.

Caloric Restriction

Caloric restriction, often shortened as CR, extends healthy, average, and maximum life spans. Various studies have analysed many short lived animals, including mice and rats, as well as animals with longer life spans such as primates. These studies follow a variety of species through a full lifespan in a shorter period of time than possible with humans. Studies on humans involve less severe parameters over shorter time spans for ethical reasons but their findings parallel those of animal studies. In published research, this method of eating is generally called dietary restriction, abbreviated to DR. Rodent studies conducted over the past 20 years have reliably demonstrated up to a 40% increase in maximum life span through life-long caloric restriction.

 Appearance of Rhesus monkeys in 
old age (approximately 27.6 years). A and B 
show a typical control animal. C and D show 
an age-matched caloric restricted animal.

The biological reaction to caloric restriction occurs in most species examined to date. It likely evolved early in the history of life on Earth as a tactic to boost the likelihood of surviving periodic famines. The effects of such dietary restrictions are the same whether you are a mouse that is alive for a few years or a human living for decades.

Unlike animal studies, in human studies of caloric restriction cannot be directly credited with the same impact on life span. We can’t directly study its effects over an entire human life span so easily and there are serious moral implications for such research. However, it has been shown provide numerous health benefits. These include lowered risks for most degenerative conditions of aging as well as improved measures of health. In recent years, more lengthy human studies of long-term and short-term calorie restriction have systematically demonstrated these benefits. Many researchers believe that the evidence to date shows the practice of caloric restriction will in fact prolong the healthy human life span. There simply isn't enough data yet to pin down the impact on an entire life span. However, it is reasonable to deduce that the impact of caloric restriction could mean a difference of 5-10 years of life.

The beneficial effects of caloric restriction in laboratory animals have been known for more than 80 years, but only in the past decade has an appreciable level of funding and attention been given to this field. There are many ways that caloric restriction benefits health, including: increased insulin sensitivity and decreased oxidative stress. It even positively alters levels of the friendly bacteria in your digestive system!

There are several different ways in which caloric restriction may work. The area that seems to get the most research is related to a family of genes called Sirtuins. There are seven mammalian sirtuins that we know of (SIRT1 through SIRT7). In the last decade, these sirtuin proteins have received a lot of attention as epigenetic regulators of aging. The growing association between ageing and neurodegeneration has led researchers to investigate the role of sirtuins as potential targets for the development of novel therapies to prevent or slow down the progression of Alzheimer's disease.

SIRT1, the most studied member of the sirtuin family, has already been shown to regulate numerous neuro-protective functions, including the antioxidant and anti-inflammatory response. It also plays a key role in the regulation of insulin, gene transcription and the production of new energy-producing mitochondria. There is a heavy research focus on SIRT1 gene expression because it can be targeted by drugs and by supplements like Resveratrol. But there is a much easier way to regulate this powerful gene expression, and it takes us back to the beginning of today's discussion.

Simply put, SIRT1 is negatively regulated by both MTOR and Insulin. This means that excessive protein consumption and excessive carbohydrate consumption decrease the expression of our longevity genes. We are complex creatures that use oxygen to create energy. This means that we are built to burn fat, and eat fat. The sensing target for fat in our diets is a hormone called leptin. Leptin acts as an up-regulator. It encourages the expression of SIRT1 in a positive direction.

There are at least four solid reasons we are built to burn fat for fuel to create energy.

1.    A sugar-burner can't truly use stored fat for energy generation, at least not until their excess glucose runs out. When there is enough sugar/glucose available in the blood, our bodies will use it preferentially over fat. Note here that we are using the term "preferentially". This does not mean sugar/glucose is more effective or efficient for energy production. On the contrary! Carbs have fewer calories than fat to make energy, so you are forced to eat larger volumes of them in order to have enough energy to go around.

2.    When someone who is highly dependent on carbohydrates for energy goes a few extra hours without eating, they become very hungry. Think of it as essentially stoking metabolic fires with kindling (energy-light sugar) and not logs of hard-wood (energy-dense fats).  Clinical studies have even shown that the body fat of even carbohydrate-based dieters will release stored fatty acids several hours after eating and during periods of fasting. This is yet another sign that our bodies prefer fat as a fuel source, even if it is our own! Carbohydrate reliant eaters are simply replacing kindling with kindling without ever using much more efficient sources of energy.

3.    A sugar-burner relies on a short-lived source of energy. Glucose will work for you if need it, but you can't really store very much of it in your body. Even a 150 pound person who's fairly trim with 12% body fat has 18 pounds of animal fat on hand to be converted into energy. Compare this to our ability to store sugar/glucose as muscle and liver glycogen. We are limited to around 500 grams or so. This means that sugar burners need to supply carbs from an external source, thus stopping the burning of any body fat for energy! What a bad trade-off!

4.    A sugar-burner will use up glycogen fairly quickly, even during moderate exercise. That is not to say that glycogen-based exercise and efforts are not of some merit. Subject to the type of physical activity, glycogen burning can be completely necessary and expected. But, it is valuable fuel. If instead, you're able to stay in an oxygen-based fat-burning mode for as long as possible you are able to save glycogen for anaerobic “all out” efforts. Glycogen stores are literally life-saving rocket fuel for running like Hell from dangerous wild animals. Sugar-adapted people are wasting their glycogen stores on efforts that fat should be able to power.

Fat as a Source of Fuel: Our Evolutionary History

Looking at metabolism through the lens of evolution, we can see that fat and protein were the dominant macronutrients, (when we were lucky enough to have any food at all). Over our two and a half million years of adaptation we have sometimes not had regular access to food, especially in the form of glucose promoting carbohydrates. This would have caused our ancestors to develop effective ways to tap their own stored body fat for energy instead of relying on a steady supply of carbohydrate. Normally, our activities would not have required the level of energy that sugar can provide. After all, we were usually not in full blown flight mode (hopefully!).  As a result, we have a very low levels of glycogen (for emergencies) compared to available fat rations in our bodies. Clearly it was primarily the fats and ketones, with small amounts of glucose generated internally through gluconeogenesis, that supplied us with appropriate levels of energy for healthy living. We would have had an occasional all-out-burst of required anearobic energy (because we could not consume oxygen quickly enough) running after, or away from an animal, but these moments would have been rare in a 24 hour day.

In Conclusion

Eating is our birthright. The importance of sugars, proteins, and fat in our diets dates back to the earliest days on the planet.  At a molecular level, it an important part of a three cornered connection to the stars involving anaerobic (based on sugars) as well as aerobic (based on fats) energy production. We are literally built to eat properly and when we follow our natural genetic preferences we are paid back with the fruits of vitality and longevity.

An important revelation here is that, despite recent arguments to the contrary, high fat diets have been shown, in human subjects, to actually increase the number of mitochondria available for energy production. This leads us to an interesting point to be covered in an upcoming post on this blog, the influence of ketogenic diets and the progression of cancer.

The Biology of Stress and Depression Pt. 7: What you can do to increase levels of Brain Derived Neurotrophic Factor (BDNF)

(These are all of the posts we have on this topic)

1st Post on Stress and Depression Why the Current Theory Fails So Often

2nd Post on Stress and Depression Cortisol

3rd Post on Stress and Depression Pregnenolone

4th Post on Stress and Depression DHEA

5th Post on Stress and Depression BDNF
6th Post on Stress and Depression: The Cholesterol/Dopamine Connection
7th Post on Stress and Depression: Increasing levels of Brain Derived Neurotrophic Factor (BDNF)

Hello again and welcome to our 7th post on the biology of stress and depression. In this post we will be discussing what types of exercise have been shown to increase levels of Brain Derived Neurotrophic Factor (BDNF). As stated in a previous post (click here to go to the post), BDNF is like fertilizer for your brain's neural circuits. If you want to learn something new, you need BDNF to help you pave those new neuro-pathways. These pathways can control something physical like how to throw a perfect spiral with a football, or something psychological like a new mindset or attitude. Either way you need to grow new circuits for your nerves in order to wire yourself for a new task. This process of creating these neurological structures or networks to adapt to new psychological, physiological, or emotional needs is called neuroplasticity.

In his book, Evolve Your Brain, Dr. Joe Dispenza eloquently described the neural network as, ".literally millions of neurons firing together in diverse compartments, modules, sections, and subregions throughout the entire brain. They team up to form communities of nerve cells that act in unison as a group, clustered together in relation to a particular concept, idea, memory, skill, or habit. Whole patterns of neurons throughout the brain become connected through the process of learning, to produce a unique level of mind."

So the term "neural network" describes a unique arrangement of connections of neurons that fire in a specified sequence. These networks allow you to perform tasks like tapping your feet, or recalling the lyrics to your favorite song as well as "learning" new tasks as required. Neuroplasticity is the ability of the brain to adapt and change. This flexibility in our nervous systems is based on the modification of existing neural networks and the creation of new ones. A key player in our ability to adapt to new nerve stimulus is a steady supply of BDNF.

If can keep optimal levels of BDNF ready to feed and develop new circuits in your brain the process of developing new skills, knowledge, and attitudes becomes much easier. So, BDNF helps you be the "you" that you want. You build yourself from the inside out firing and re-wiring new pathways based on what you choose to focus on. The implication here is that each of us an unexpected degree of control over who we are and how we feel.

The previous post on the stress hormone cortisol discussed the inverse relationship with cortisol has with cortisol production. If stress hormone and cortisol levels go up levels of BDNF go down. Cortisol also decreases the body's ability to deal with stress. It does this though damaging the hippocampus, a major contributor in the body[s ability to adapt to stress. As a result we feel stress more acutely even as the body has become even less able to cope!  It's a really strong feedback loop that encourages us all to be stressed. The good news is this nasty little equation can be reversed. By increasing BDNF we can decrease damaging levels of cortisol. This is how you re-wire to the new you that you want to be.

Our first look at increasing BDNF is exercise.

While our muscles pump iron, our cells pump out something else: particles that nourish a strong brain. For years scientists have struggled to explain the well-known mental benefits of exercise. These benefits include a variety of paybacks, including: offsetting depression and aging, to fighting Alzheimer's and Parkinson's disease. And, a team of researchers may have finally discovered a solid molecular link between how a good workout promotes a healthy brain.

Muscle cells increase the production of a protein called FNDC5 while you are exercising. A portion of this protein, called irisin, gets cut off and released into the bloodstream. Spiegelman and his colleagues at Harvard Medical School suspected that FNDC5, and the irisin created from it, are responsible for exercise-induced benefits to the brain. In particular they were interested, (as are we!), in increased levels of BDNF.

To sort out how exercise relates to BDNF, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. They put an experimental group of mice on a 30-day endurance training regimen. They didn't have to coerce their subjects, because running is part of a mouse's natural foraging behavior. The mice with access to a running wheel ran the equivalent of a 5K every night. Next, they compared them to a group of mice who lived like couch potatoes.

Aside from physical differences between wheel-trained mice and sedentary ones, (not surprisingly, the sedentary group had more body fat), the groups also showed significant neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory. A happy hippocampus is also associated with better stress management and less depressed states.

Using mouse brain cells developing in a cell culture, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results in the journal Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. The processes parallel each other! The mind and body are not separate after all.

How is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it's also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse's bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain. This research finally sheds light on how exercise relates to BDNF and other so-called neurotrophins that keep the brain strong and healthy.

We have come a long way in the past twenty-five years in our understanding of the brain, from a generally accepted perception of the brain as being a hardwired, fixed and immutable organ to one that celebrates its dynamism. Now get out there and move it!

The Biology of Stress and Depression Pt. 6: The Cholesterol/Dopamine Connection

(These are all of the posts we have on this topic)

1st Post on Stress and Depression Why the Current Theory Fails So Often

2nd Post on Stress and Depression Cortisol

3rd Post on Stress and Depression Pregnenolone

4th Post on Stress and Depression DHEA

5th Post on Stress and Depression BDNF
6th Post on Stress and Depression: The Cholesterol/Dopamine Connection
7th Post on Stress and Depression: Increasing levels of Brain Derived Neurotrophic Factor (BDNF)

The sixth installment on the biology of stress and depression turns to research on cholesterol and its relationship to emotional states. For some people, the information presented here may come as a bit of a shock.  There are strong indications in current research that cholesterol has very little to do with heart disease. There have been several books written on this problem that go into great detail. My own work can be found here (click link). The footnotes nested in the text are particularly valuable to anyone researching the subject.

In short, cholesterol by itself is not bad for your health. Cholesterol is involved in basically every process in the body given that various parts of individual cells are made up of cholesterol.  Given the amount of research available, this post is not going to spend much time defending the position that cholesterol is helpful and not harmful. It is, however, going to explain the vital role that cholesterol plays in your emotional stability.

Several years ago, there was a paper published in the Journal of Psychiatric Research.  The research followed just shy of 4, 500 veterans for 15 years. At the end of the study they made an in interesting finding that participants with LOW total cholesterol numbers who concurrently were suffering from depression were SEVEN TIMES more likely than other subjects to die prematurely from unnatural causes such as suicide and accidents! This work basically got no attention from the media. Most medical doctors were likely to dismiss the study as well. Why? (A closer look at this WHY question can be found by following the link above)

For years scientific research has noted the problematic relationships between low cholesterol, depression, and an elevation in problems with impulsive behaviors. For example:

1.       A study published in the Journal of Behavioural Medicine observing men aged 40 to 70 found that the men with long-term, low total cholesterol levels "have a higher prevalence of depressive symptoms" when compared to subjects with higher cholesterol levels.

2.       A 1993 study in the prestigious journal The Lancet reported, "Among men aged 70 years and older, categorically defined depression was three times more common in the group with low total plasma cholesterol...than in those with higher concentrations..."

3.       Women with low cholesterol levels are also vulnerable to depression. A Swedish study, also published in the Journal of Behavioural Science, involving 300 healthy women, aged 31 to 65, concluded that women in the lowest cholesterol group, the bottom ten percent, suffered from significantly more depression symptoms than the other women in the study.

Unfortunately, a diagnosis of depression is often associated with a higher risk of suicide. The link between suicide and low cholesterol is also well supported

1.       The results of a 2008 study of hospitalized psychiatric patients published in the journal of clinical psychiatry suggested that low cholesterol may be associated with suicide attempts.

2.       University of Minnesota from the Archives of Internal Medicine found that people with total cholesterol levels lower than 160 mg/dL were more likely to commit suicide than those with higher cholesterol levels.

3.       As published in Progress in Neuro-Psychopharmacology and Biological Psychiatry, cholesterol and blood fat levels were found to be lower, on average, among patients with bipolar disorder who had attempted suicide than bipolar patients who had not.

 So, where is the connection between depression and low levels of cholesterol? Research from the Karolinska Institute has found that a healthy dose of oxidised cholesterol (known as oxysterol) is indispensable in promoting the development of the human stem cells that make dopamine. For those who don’t know, dopamine is a big player in the chemistry of our nervous systems. A huge variety of illnesses are associated with upsets in dopamine levels.

People with Parkinson’s disease experience the death of the dopamine producing neurons in the substantia nigra regions of the brain and this leads to general shaking in their bodies. People with ADHD, (Attention Deficit Hyperactivity Disorder), strive unsuccessfuly to supply their brain with enough dopamine to focus. One of dopamine's functions is to kick start us. It is a kind of chemical motivator. It is actually small bursts of dopamine that make us want to actually get up and DO stuff. 

Our brains are big on cholesterol! It is a primary building block of our brain cells and without it they literally die off. But in addition, as this article emphasizes, cholesterol is a primary contributor to the production of dopamine and dopamine is what makes us motivated and forward thinking. Dopamine is the currency of the reward center in our brains.

We usually think of dopamine as linked more with things like reward or drug-addiction, but the list of things dopamine actually does is more complex than that. Dopamine is involved in movement, for example, but it is also involved in, for lack of a better word, “motivated behavior”. Think of dopamine in terms of “salience”. In other words, it helps to determine how relevant something is to your interests. Its effects encompass all motivated behaviors for things such as food, sex, drugs, etc. as well as the development of major depressive disorder. People with depression often exhibit reduced motivation, anhedonia (a decrease in pleasure from usually enjoyed things), as well as possible decreases in motor function.  

All of these difficulties can be linked to incorrect levels of dopamine. So targeting the dopamine system is one of the ways in which we can look at potential mechanisms and treatments for depressive behaviors.

Cholesterol is also the precursor to the neurosteroids we discussed in previous postings (DHEA & Pregnenolone). Low cholesterol means low output of those vital sparks that keep our nerves happy and active.

The research noted in this and previous posts suggests strongly that cholesterol is incredibly important in the stability of mental health. It is a key to the production of dopamine. Dopamine is central to bodily movement & “wanting things” like: new experiences, new possessions, new potential mates and a future. All of this begs the question of whether knee jerk use of medications and alterations in diet designed to decrease cholesterol levels are actually a wise idea. 

The Biology of Stress and Depression Pt. 5: BDNF

(These are all of the posts we have on this topic)

1st Post on Stress and Depression Why the Current Theory Fails So Often

2nd Post on Stress and Depression Cortisol

3rd Post on Stress and Depression Pregnenolone

4th Post on Stress and Depression DHEA

5th Post on Stress and Depression BDNF
6th Post on Stress and Depression: The Cholesterol/Dopamine Connection
7th Post on Stress and Depression: Increasing levels of Brain Derived Neurotrophic Factor (BDNF)

Hello everyone and welcome to our 5th post on the biology of stress and depression ...

What if there were a way to help promote the growth of new nerve cells and tissue? Until recently, medical science in general thought that we grow all the nerve cells that we can grow
unitl we hit adulthood. After that, the best we could expect is a slow degeneration of our mental capacity and nervous system. Well, it turns out that these theories were missing a crucial factor in brain function called "brain-derived neurotrophic factor" or BDNF.

BDNF activates brain stem cells to convert into new neurons. BDNF also triggers numerous other chemicals that promote neural health. Inappropriate levels of BDNF have been found to be related to a host of mental health problems, including: Alzheimer's disease, schizophrenia, epilepsy, drug addiction, and of course depression.

Previous posts highlighted the impact of chronic stress on the brain.  Elevated stress destroys a part of the brain called the hippocampus. The hippocampus acts as a brake on stress responses. Poor hippocampal function leads to increased responce to stress and consequently more damage to the brain. It was also noted that elevated stress hormone levels decreased the neuro-protective-hormones DHEA and Pregnenolone. DHEA and Pregnenolone have been studied, and found effective, in the treatment of various chronic stress and depression models with human subjects. Both of these hormones have strong mood-regulating effects.

This post asks whether there is a relationship between levels of the stress hormone cortisol and BDNF? Yes! Elevated cortisol levels lead to a decrease in BDNF. Indirectly, stress reduces the effectiveness of neurochemical connection within brain. This reduction leads to impulse control issues, a lack of learning capacity, and memory problems. In fact, since intestinal bacteria are directly related to the production of BDNF, (as discussed later in this article), reduced levels even explain why people who are depressed usually have poor appetites. BDNF puts an actual face on the vague symptoms of the DSM (Diagnostic and Statistical Manual) criteria used for diagnosing depression. Clearly, regulating BDNF production can help people who are stressed or depressed.

The point of this posting is that you CAN learn new behaviors, and you CAN grow new neural circuits to help build a better functioning brain. The end result is life.  The key to this change is producing healthy levels of BDNF and lowering levels of stress hormones like cortisol.

How do you do this? Is there a drug or a magic bullet that can bring about positive changes in the relationships between these seemingly magical chemicals in the body? The answer is yes - BUT - the magic bullet is a strategy not any one particular thing. We can only imagine what people think when they realize that they can be happy and healthy again. It takes a little bit of effort, and a few small lifestyle modifications, but success is achievable.

Five Ways to Increase BDNF

Avoid sugary beverages ... esp. if they have health claims ... 

1.       Avoid fructose.  No, we aren’t talking about fruit here. We are talking about packaged/bottled foods sweetened with fructose. These may also be called “added sugars”.  Fructose has been shown to suppress BDNF secretion in several studies. Packaged foods are generally devoid of nutritional value anyway. Buy actual fresh food and enjoy the benefits!

2.       Exercise has been shown to have dramatic impact on BDNF production. Multiple studies have found that moderate levels of exercise lead to a significant improvements in BDNF production. Further, moderate exercise has also been shown to elevate levels of sex hormones and decrease stress hormone levels. Moderate weight lifting and low level cardio is what we are talking about. High intensity cardio does the opposite and increases stress hormones and lowers sex hormones. However, exercise of either intensity has a positive effect on BDNF.

3.       Chinese Herbal medicine has several formulas that directly increase BDNF levels.  One medication in particular, Yue Ju Pills, is supported by some very promising research.  In published studies, this formula has been found to have multiple anti-depressant actions beyond just increasing BDNF.  Interestingly, this Yue Ju Pills (first described in 1281 AD) were traditionally used to treat depression and irritability. It is no exageration to say that it has stood the test of time.

4.       Meditation has long been known to be a positive behaviour for people with depression.  Regular meditators have lower levels of the stress hormone cortisol, and higher levels of BDNF.

5.       Omega 3 fats have a positive effect on BDNF levels, no surprise there since they are so heavily related to a healthy brain.  There are plenty of sources, both plant and animal, of omega 3 fats. These sources include: fish, grass-fed beef, flax seeds, chia seeds & sacha inchi seeds.

There it is … a simple and relatively easy to follow strategy to a healthy and flexible mind.  The real key is getting out there and doing it!  There will be further posts detailing each of these steps, but, knowledge is only power if you use it!

Get out there and enjoy life!




Stay Tuned!

Yours,

David

The Biology of Stress and Depression Pt. 4: DHEA

(These are all of the posts we have on this topic)

1st Post on Stress and Depression Why the Current Theory Fails So Often

2nd Post on Stress and Depression Cortisol

3rd Post on Stress and Depression Pregnenolone

4th Post on Stress and Depression DHEA

5th Post on Stress and Depression BDNF
6th Post on Stress and Depression: The Cholesterol/Dopamine Connection
7th Post on Stress and Depression: Increasing levels of Brain Derived Neurotrophic Factor (BDNF)

Welcome to the fourth post on the biology of Stress and Depression.  Just to recap important information from the previous posts, please review the following:

The current model regarding the problem of depression (that most medical providers believe) sees it as a lack of neurotransmitters (dopamine, serotonin & nor-adrenaline). This view sees depression as a “lack of happiness”. If you want to treat a depressed patient, you give him/her drugs to increase the presence of these deficient hormone(s). Increasing amounts of these hormones should, in theory, make people happier. The trouble is that in the light of other explanations of depression, this theory is very limited.  In addition, it does not take into account the impact of stress on the body.

Current research clearly shows us that stress leads to depression.  Excessive amounts of stress lead to the gradual destruction of the hippocampus.  The hippocampus controls the body's reaction to stressors. Increasing amounts of stress and the consequential destructive impact on the hippocampus lead to a reduced ability to handle further stress. It can become a vicious cycle.  That cycle is reinforced by research finding that untreated stress/depression is linked to having a smaller hippocampus which in turn is directly linked to being predisposed to depression. This is largely because of reduced ability react appropriately to stressors.  Clearly, stress does lead to depression. 

Note: stress is often regarded as something people have control over. This is often not the case.  Stressors are not just series of thoughts. Stress can be biological or physical in nature and either is often completely out of our control.  In order to cut depression off at the source, we need to find ways to deal with all forms of stress. 

In the previous post we discussed a neuro-hormone with anti-depressant properties called pregnenolone. In this post we will be discussing another important neuro-hormone involved with stress and depression called DHEA.

DHEA is an abbreviation for dehydroepiandrosterone. Levels of DHEA peak in your 20's and slowly fall as you age. By the time you reach 40, your body makes about half as much DHEA as it used to. By 65, levels drop to 10 to 20 percent; by age 80, it plummets to less than 5 percent.

DHEA is a hormone made primarily by the adrenal glands. Hormones are chemical messengers that affect the function of cells and tissues all over the body. DHEA and cortisol are long-acting stress hormones and they are inversely related to each other. If one of these hormones goes up, the other goes down. They also have opposing functions.  Where DHEA has an anabolic or regenerating influence, cortisol has a catabolic or degenerating effect. Both of these hormones are indispensable, but they must be in proper balance for optimal health. How does the relationship between these hormones become unbalanced? The short answer is "stress maladaptation".

Stress maladaptation refers to an inappropriate response to prolonged stress. The typical reaction of the body to a stressor is to produce adjusted amounts of both cortisol and DHEA. When the stress is gone, the body readjusts its output of both cortisol and DHEA to resting levels. Both return to an appropriate baseline. This is what happens with short episodes of stress. However, when the stress is prolonged, the body begins to increase levels of cortisol while reducing levels of DHEA.  How long does it take for this to happen? One study showed that after just 28 days of constant stress, cortisol levels had climbed to 240 percent and values for DHEA had dropped to 15 percent of original levels! What's worse is that even after the stress is removed, the body sometimes does not recover and bring these hormones back to normal baselines. Instead, it remains in the stress response mode with high cortisol production and low DHEA output.

Remember, stress and its ever present partner cortisol shrink and erode your hippocampus.  A happy, healthy and large hippocampus is a major factor in avoiding depression.  Poor stress management and the resulting DHEA deficit are a major factor in depression.  In fact, DHEA supplementation has been shown to promote neurogenesis (regrowth of new nerve tissue) in the hippocampal regions of rats which have been artificially stressed with high levels of injected cortisol. 

Multiple human clinical studies have also shown that DHEA effectively treats depression:

1. The National Institute of Mental Health studied 46 patients age 40-65 with major and minor depression. After six weeks of administering DHEA, 23 patients showed a 50% reduction in depressive symptoms. Ten patients chose to continue taking DHEA for one year at a low dose and remained free of depression.

2. Ten elderly men (58-69 years old) with a range of age-related symptoms such as feeling weak and having low-energy showed significant improvement in symptoms after taking 25 mg of DHEA every morning for one-year. 

3. In a 1999 study published in Biological Psychiatry, researchers tested the effects of DHEA in 15 people who had developed mid-life depression. Sixty percent of those receiving DHEA responded well to treatment compared to only twenty percent of those who received the placebo.

4. In a large-scale study conducted in 2007, of 2,855 elderly men and women, it was concluded that low DHEAS levels were linked with depressive symptoms.

5. A 2007 study of sixty-one patients with Dysthymic disorder (DD), a chronic state of mild depressive symptoms, found that individuals with DD have low levels of DHEAS.

A  2009 comprehensive review of DHEA in the treatment of depression concluded:

"... to date, every controlled trial of DHEA in depression has reported significant antidepressant effects."

Managing cortisol is becoming a major factor in the treatment of stress and its resulting depression.  There is more research to be done, but to be honest, no matter where one looks, there is always more research that needs to be done.  The results from the above list of studies is already more impressive than the results of traditionally approved drug treatments for depression.

Does this mean you should run out and supplement with DHEA without guidance from a health care provider?  No.  DHEA is a hormone, not a vitamin.  But the clinical results show that this treatment will help some of those not helped by their current anti-depressant medications.

In our next post we will be discussing Brain Derived Neurotrophic Factor …

Stay Tuned!

Yours,

David

A Brief Introduction to Qi Gong Meditation

A Brief Introduction to Qi Gong Meditation

A Younger David at 23

Understanding the Process:

There are steps that must be learned in proper Qi Gong breathing. All of these steps work in concert with each other. The steps which are outlined in this article will help you absorb the most out of the air you breath. Each step helps maximize the amount of time your lungs are exposed to the life giving elements in air, these steps also help increase the surface area you have in your lungs to absorb these elements into your blood stream.

Posture:

Let’s start with a picture, since it is much easier to show posture than to explain it.

You want your head over your hips and your spine straight but relaxed.  This can be kneeling, cross legged or seated in a chair.

The Four Stages of Breath

Inhale
Condense
Exhale
Pause

Inhalation should begin with empty lungs and flared nostrils. Fill your navel area first. Think of filling your lungs like pouring water into a cup, the bottom fills first. Do not make the mistake of many people beginning Qi Gong and only try to fill the bottom. Continue to fill the middle and upper portions of your lungs as well. Do not over fill your lungs, comfortably fill them. The idea is to expose the entire surface area of your lung to the air you inhale.

Condensing the air in your lungs is fairly simple. Just slightly push it downward toward your navel and imagine energy being absorbed through the lung and into the body.

Exhale the air in your lungs smoothly, and again, with flared nostrils. There should be a smooth transition between each phase. Make sure you exhale the lower sections of your lungs, but do not force the air out, just let it happen. If you are in a rush to inhale you’ve condensed the air for too long.

A pause should happen at the end of each breath. This makes your blood circulate and removes stagnation. Take this time to check your posture and relax your abdomen for the next breath.

The Locks

The Lower Lock
The Throat Lock
The Abdominal Lock

These techniques are considered locks in terms of energy, but they are more contractions from a purely physical view. It is very important to apply these locks because they help you look inwardly. They also help you condense the energy you are harvesting from the air, and seal them from leaking out. Each lock has it’s own place in between a stage in the four stages described above.

The Lower lock, also called the anal lock, is the first lock to be applied during Qi Gong Breathing. Apply this lock as you begin to reach a comfortable capacity for your inhalation. You should tighten the outer ring of the anal sphincter, which will stimulate the nerves of the sacrum. This is your first step in stimulating the Qi to raise from the sacrum to the brain. It is also important because this provides a firm foundation for breath compression.

The throat lock is applied when you have reached a comfortable full inhalation . This is nice and simple, all you need to do is simulate swallowing. This will stop any air from leaking out from the upper portions of your lungs. Also, this will provide a firm ceiling for your breath compression.

The abdominal lock is simple as well, all you need to do is relax your abdominal muscles and draw your navel in slightly toward the spine. This step is the last in the three locks, it is also the most important. In building up your internal energy you should focus on your lower abdomen, or Dan Tien in Chinese.

These processes could easily be compared to compressing a large pile of shredded paper. You want to take something that is light and thin, and compress it into something solid and strong. Again, this all seems complicated when you start but after a few weeks or months it becomes natural and easy. My teacher likened many of these processes to driving a car. At first you need to clutch, shift, brake and check your mirrors, but soon it becomes natural.

Yours,

David