Anxiety.

Anxiety is very common.

It is the most dominant kind of mental disease in the US. Anxiety affects more than 40 million individuals or 18% of the population. However, only about a third of people suffering from this condition seek treatment. Anxiety and depression frequently overlap, with roughly half of the depressed people also having anxiety.

In my practice, part of what I will discuss when explaining treatment options is the important role of diet in managing all types of mental illness. It is a root cause of most mental illnesses that are not genetic if there are no underlined phycological traumas or issues. In most cases, depression is caused by chronic inflammation in the brain.

In addition to healthy guidelines such as avoidance of psychoactive substances and limiting or avoiding alcohol and caffeine, there are many other dietary considerations that can help relieve anxiety. For example, complex carbohydrates are metabolized more slowly and thus help maintain a more even blood sugar level. If you are suffering from chronic hypoglycemia attacks you are also suffering from post-traumatic stress disorder. When sugar drops below normal levels your brain cells begin to die off and this triggers survival mechanisms that if not corrected could leave to post-traumatic stress disorder. In experimental conditions with mice, this has been shown repeatedly.

Oxidative Stress and Neuroinflammation.

There is growing evidence that chronic inflammation in the brain may be associated with the development of a wide range of neuropsychiatric disorders. This includes not just classical cognitive decline but other neuropsychiatric disorders like depression and anxiety. This is a consequence of a pro-inflammatory diet that causes an imbalance between oxidative stress and the antioxidant defense system in the brain.  

Major depression and anxiety are currently associated with a lowered total antioxidant state.

The standard antidepressants that will be prescribed to patients with major depression may also produce beneficial effects outside of the regulation of neurochemistry. It is proven in research that most antidepressants act as antioxidants in the brain and one of the therapeutic effects they exhibit is normalizing the damage caused by oxidative stress. Most of these medications also come with serious side effects.

In recent years there was a wide range of studies that correlated and explained the role of oxidative stress-induced neuroinflammatory response, mitochondrial dysfunction, neuroplastic deficits, and intracellular signaling pathways in the development of depressive and anxiety disorders. Today this is accepted science.

Chronic inflammation as a result of oxidative stress is also correlated to neuropathies. Chronic inflammation damages all types of major groups of cellular macro-molecules not just proteins but also lipids, carbohydrates, and nucleic acids. All of this damage will eventually lead to DNA damage, mutation and cancer or cell death and cognitive decline, and neuropathy.

Metabolic rate.

Why this happens in the brain more than other organs because of the high demand of the brain for oxygen. Our brains use 20% of all the calories we eat and 20% of the oxygen we breathe. Bear in mind that a brain weighs about three pounds. This means that the metabolic rate of the brain cells is higher than other cells in the body. Deprived of oxygen brain cells die quickly.

Even the smallest imbalances in antioxidant defense mechanisms can be lethal to neurons. Because we have a limited amount of brain cells even the smallest imbalances in antioxidant defense mechanisms will lead to extensive damage if the imbalances are chronic. This also leads to imbalances in brain neurochemical processes and is correlated to depression and anxiety.

Blood-brain barrier.

The nervous system is rich in iron and fat. Iron is very reactive and oxidizes quickly. Fat, especially unsaturated fats are also very reactive to oxygen. These factors render tissues more vulnerable to oxidative damage, as do the high metabolic activity and abundant blood supply.

In a situation where most of the population is vitamin E deficient, this would translate into an increase in neuropsychiatric disorders.

The second and main problem that underlines all of the oxidative damage outside of direct nutritional deficiencies is something known as the blood-brain barrier. If you are low on vitamin E some other fat-salable antioxidant might neutralize some of the free radicals but in the brain, it is a different story.

Because neural cells are extremely sensitive and require a pure environment to function effectively, the brain has to defend itself from toxins and undesired substances far more than the rest of the body. As a result, there is a blood-brain barrier that keeps a lot of toxic substances out. At the same time, it keeps a lot of antioxidants out as well.

Only lutein and zeaxanthin from more than 20 dietary carotenoids that can be found in the bloodstream will go through the blood-brain barrier. Astaxanthin is a third one.

They are also present at the highest level of accumulation inside the body. It appears that the brain and retina both actively collect xanthophylls. Lutein is a dominant one. It is likely that low lutein consumption would result in age-related brain and macular degeneration.  Much more than other carotenoids.

The Role of Antioxidants in Depression: Clinical Evidence.

In spite of the fact that antidepressants increase oxidative status, and this includes almost all of them that are in use in clinical practice, the complete mechanism of antidepressant action is still not fully explained. The typical theory was formulated around the idea that antidepressants restore neurotransmitter levels to normal and this is a primary theory. They also exhibit antioxidant effects and this is considered to be a secondary effect.

Lithium and valproate, two common medications for bipolar disorder, also have antioxidant qualities.

Supplementation with antioxidants in trichotillomania, a condition related to obsessive-compulsive disorder (OCD), also reported significant improvement in symptoms.

The levels of MDA were dramatically reduced by the selective serotonin reuptake inhibitors (SSRIs) fluoxetine, sertraline, fluvoxamine, paroxetine, and citalopram. Malondialdehyde (MDA) is an end-product formed during oxidative stress, concretely lipid peroxidation. For example, in animal models the increase in brain level of MDA after endotoxin administration was decreased by the lower dose of fluoxetine. At the same time, fluoxetine increased glutathione, suggesting that it has an antioxidant effect on the brain.

Mitochondria is also a prime target for oxidative damage. The role of mitochondria is to burn oxygen or in other words oxidative phosphorylation. This creates energy in form of ATP. Mitochondrial dysfunction is the loss of efficiency in the process of ATP energy production due to oxidative damage.  It is considered to be a normal part of the aging process and is effectively correlated to all known chronic diseases including cancer, cardiovascular diseases, and neurodegenerative diseases.

Inhibition of the mitochondrial MAO is one of the most studied effects of antidepressants. MAO activity contributes to mitochondrial dysfunction. Patients suffering from depression, panic disorder, and other anxiety disorders appear to respond well to both selective and nonselective MAO inhibitors. Antidepressants, which primarily function as reuptake inhibitors of serotonin and/or norepinephrine, also inhibit MAO, bringing more validity to the concept of antioxidant action in the treatment of depression and anxiety.

While to a considerably lower extent than in the case of animals, the relationship between anxiety and oxidative stress has been researched in humans as well. Most of the studies were constructed in a way to see if some dietary antioxidants might be prescribed as supportive therapy to standard medication.

The Role of Antioxidants in Anxiety.

My recommendation will be to choose high antioxidant-rich food choices if you can. If you want to eat salad eat kale instead of lettuce. If you want to eat fruit eat berries instead of bananas. If you want a beverage drink hibiscus tea instead of Coke. If you have some pro-inflammatory condition this will improve your health significantly. There are many diseases out there that are caused by inflammation but many people don’t know that they are caused by a bad pro-inflammatory diet.

Depression is just one of them (2). For some people, it is bad genetics that plays a role, but for some, it is a bad diet and in both cases, antioxidant-rich food will help. If you suffer from mood disorders disregard USDA recommendations and eat as many antioxidants as you can.

“Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of mood disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces ‘sickness behavior’ resembling depressive symptomatology. Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity, and structural and functional brain changes. Anti-inflammatory agents, such as acetylsalicylic acid (ASA), celecoxib, anti-TNF-α agents, minocycline, curcumin, and omega-3 fatty acids, are being investigated for use in mood disorders. Current evidence shows improved outcomes in mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy.“

This makes sense if we understand how evolution works. If depression does not have an evolutionary protective role for the species it will be selected against. The high rate of mood disorders in our current society is a consequence of adaptive benefits. The problem is a shift in environment and diet.

Depression as an evolutionary protective strategy.

The theory goes that depression is an evolutionary strategy for infection control.

If you have a life-threatening virus you will be put into isolation to prevent the spread of infection. Depression does the same thing. In the stone age for example infection was a leading cause of death and more than half of the children died before reaching puberty. Life expectancy was 25 years of age. The theory was made that if one individual gets influenza or some other life-threatening disease the instinct of that individual will be to become irritated, depressed, and antisocial on top of all of the visible signs of sickness.

It is not the pain that causes depression but overall inflammation.

This is bad for individuals but if we look at the overall survival of the species it is beneficial. Individuals that have some sort of health issues and that have inflammation no matter what source of that inflammation might be, will as a theory goes suffer from the additional shift in brain chemistry. That will make them depressed, irritable, and angry as an instinctive underlying mechanism. The purpose is to isolate that individual until the infection is gone so that the spread of infection is minimized.

But what happens if the source of that infection is not some life-threatening virus but a bad and pro-inflammatory diet?

There are animal species like honey bees that will leave to die alone if they are sick. This is not something new. This connection was well known for almost a hundred years now. If doctors give people drugs that induce inflammation depression will be induced as well.

More than 50 percent of people that receive interferon develop severe forms of clinical depression.

Lacking an adequate level of antioxidants in a diet plus the addition of all environmental toxins plus dead meat bacteria endotoxins will be pro-inflammatory and depression-inducing. Endotoxins are part of the outer membrane of the cell wall of gram-negative bacteria. They are released from bacteria when they die, their cell walls get destroyed and cannot be cooked away any further. There are a lot of dead bacteria in meat and this is one of the reasons why meat is so pro-inflammatory on top of other factors. We can cook the meat but endotoxins will remain. In experiments done in vivo after injecting endotoxins directly into human subjects, the autoimmune reaction and inflammation were significant and have led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood.

Also, other experiments proved this through brain imaging. In people injected with endotoxins brain imaging showed a lack of normal excitement to pleasurable stimulation known as anhedonia.

Inflammation changes reward-related neural responses in humans forcing us to become nonresponsive to pleasurable stimulation where we will need stronger stimuli to exert the same effects and then this can create pleasure-seeking behavior, binge eating, and depressed mood.

My recommendation to patients that have any type of mood disorder In addition to healthy guidelines is to try to remove pro-inflammatory foods from their diet and includes all animal products plus a wide range of other vegan products as well and then to dramatically increase the ORAC units score of their diet. Also, you will need to correct vitamin E deficiency, take supplemental astaxanthin and increase lutein and zeaxanthin consumption (kale and spinach).

Conclusion:

• Anxiety is very common.
• Anxiety and depression frequently overlap.
• In most cases, depression is caused by chronic inflammation in the brain.
• If you are suffering from chronic hypoglycemia attacks you are also suffering from post-traumatic stress disorder.
• Major depression and anxiety are currently associated with a lowered total antioxidant state.
• It is proven in research that most antidepressants act as antioxidants in the brain and one of the therapeutic effects they exhibit is normalizing the damage caused by oxidative stress.
• Chronic inflammation as a result of oxidative stress is also correlated to neuropathies.
• Even the smallest imbalances in antioxidant defense mechanisms can be lethal to neurons.
• Only lutein and zeaxanthin from more than 20 dietary carotenoids that can be found in the bloodstream will go through the blood-brain barrier. Astaxanthin is a third one.
• Depression is an evolutionary strategy for infection control.
• It is not the pain that causes depression but overall inflammation.
• More than 50 percent of people that receive interferon develop severe forms of clinical depression.
• In people injected with endotoxins brain imaging showed a lack of normal excitement to pleasurable stimulation known as anhedonia.
• Inflammation changes reward-related neural responses in humans forcing us to become nonresponsive to pleasurable stimulation where we will need stronger stimuli to exert the same effects and then this can create pleasure-seeking behavior, binge eating, and depressed mood.
• Patients that have any type of mood disorder need to remove pro-inflammatory foods from their diet and that includes all animal products plus a wide range of other vegan products as well.
• Patients that have any type of mood disorder need to dramatically increase the ORAC units score of their diet.
• Patients that have any type of mood disorder need to correct vitamin E deficiency, take supplemental astaxanthin, and increase lutein and zeaxanthin consumption (kale and spinach).

Passages selected from a book: “Go Vegan? Review of Science: Part 3” [Milos Pokimica]

1. Novel Therapeutic Targets in Depression and Anxiety: Antioxidants as a Candidate Treatment doi: 10.2174/1570159X11666131120231448
2. Inflamed moods: a review of the interactions between inflammation and mood disorders. doi: 10.1016/j.pnpbp.2014.01.013
3. Depression as an evolutionary strategy for defense against infection. doi: 10.1016/j.bbi.2012.12.002
4. Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood doi: 10.1016/j.bbi.2009.12.009
5. Inflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward. doi: 10.1016/j.biopsych.2010.06.010

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