Depression : Is it seratonin or SSRI deficiency? (Part 2)

As we have witnessed in recent years (till present time), there are much more cases of mental disorders amongst the population. From depression to bipolar disorders and even ADHD which is common with children nowadays, how often we ask ourselves why is this happening? Instead of popping pills like candies without proper extended diagnosis and functional investigation in a more holistic approach, the medical condition diagnosis and treatment look hopeless and broken. In this case, we are referring to mental health and depression.

As we walk into a doctor's office, most of the patients have less then 30-45 seconds before the medical doctor interrupt you and reach for that prescription pad. How often does a medical doctor really listen to a patient? Not to mention thorough assessments and find out about your digestion, sleep quality, hydration, movement or even diet and nutrition. The problem is, most conventional medical doctors are not trained to do such investigation and assessments, and legally speaking, these medical professionals are concern of being sued or stripped off their doctors' licenses if practice any other approaches which is against the code of conduct or agreement. 

In today's post, let's discuss how certain genes may play a vital role in susceptibility of mental disorders or depression. Before we continue, or if you are on SSRI medications, please take note that this is NOT a medical advice nor treatment. Do consult your medical doctor for advise before you take any action yourself. Although the facts presented here are primarily based on research and literatures, always work with your medical doctor especially if you are on anti-depressant drugs. 

As we have all heard about how genes may affect our body and health and susceptibility of diseases and medical conditions, how much truth in that? Well, according to the largest human genetics research (The Human Genome Project), the scientists have concluded that our genes could affect our health and susceptibility of disorders or diseases, but only 5% in most individuals. In a minority, some people may inherit up to 10% of gene makeup from their ancestors. What does that tell you? Does it mean that you are born to develop diabetes or depression? Do you have to give up your life because your parents or grandparents died of heart disease or cancer? Of course not. Yes, if you inherit certain genes which may increase the susceptibility of certain medical conditions, you can still take control of your life and health, by determining and controlling other variables and factors in life, such as diet, environmental stressors, stress levels, toxins exposure, exercise, etc.

As it is easy to give up on taking control and ownership of our lives, blaming others and playing the finger pointing game, many of us are living in  'Child's mind in an adult's body'. These individuals tend not to take responsibility of their lives and bodies, and often stay in comfort zone in most of the time, looking for quick fixes and ignoring what is happening around them and not listening to the body's signs and symptoms. 

Now, let's bring up the discussion of MTHFR. For most people, it is something new, but in the field of medicine, more and more medical doctors are aware of this, thankfully. MTHFR genetic mutations has been critical in terms of susceptibility of long list of diseases including depression and other mental/neurological disorders. This will be one of the three genes I will discuss in this post today.

What is MTHFR? Well, you can google many different websites with similar elaborations and explanation what it is all about. Yes, I have to admit that the entire MTHFR understanding is very complex, but I will try to make it easy to understand for you readers out there. Before I continue, let me make it clear that I'm NOT the expert of this field. Based on my own intensive research and reviewing literatures conducted on MTHFR, I'm hoping to share this important awareness to more people especially my own clients. 

Let's think of it as 2 different phases of 'ball passing' for the entire MTHFR process to complete successfully. The methylation process in the body is so complex, that I think intensive and thorough research with hours and hours of reading medical journals is required to fully understand how it actually work. the acronym of MTHFR is methylenetetrahydrofolate reductase. Forget about the scienfitic name, but you have to realize that folate is the key nutrient needed to produce the end phase of methyl-folate before being passed on to 2nd phase. 

Please take note that we are still discussing about how MTHFR could affect mental health and depression. Although there are other long list of medical conditions such as cancer, heart disease, autoimmune disease, etc which are more susceptible if one inherit one or two of the copies of MTHFR mutated genes.  If an individual inherit one copy of the mutated genes, he or she is associated with 30-40% of reduced capacity of enzymes activity for the body to do its job. And if you inherit both the mutated copies of MTHFR genes, the association is 60-70% and that's bad news. 

Let's zone in abit on phase 1 for MTHFR process. Think of walking down the stairs or passing the ball from one end to the other. There are few (primarily 5) steps in phase 1 prior to successfully making the end product of methyl-folate. Think of first step of the stairs where folate needs to bind to its receptors and making its way to final step in order to successfully become active form of methyl-folate. The are other factors why certain people unable to successfully produce sufficient amount of methyl-folate in the body. One of the reasons are due to synthetic supplement form of folic acid. Most people have heard of this nutrient as it is prescribed by medical doctors to patients especially women. Bear in mind, folic acid is NOT recognized by the body and is not bio-available. None of us should be taking this synthetic form of supplement. Folic acid from supplements will block the receptors of folate in the cells and disabling natural folate from binding into its own receptors. This will cause problems as it will reduce the body's capacity to produce the end product of methyl-folate.

You must be asking, "What if my doctor tell me to take folic acid?" Well, do your homework and research, bring the concern to your doctor and work with him. Always remember, your doctor is suppose to work with you on your medical condition, and you have every right to fire your doctor if you feel he or she is incompetent and refuse to look at the medical literatures you are presenting right in front of him.  

Now, assume that your body can make methyl-folate with flying colors, you still need another nutrient called Methylcobalamin (B12).  Both of these bio-available B vitamins are then passed on to next phase with involved SAMe. What is SAMe? First of all, it is a powerful natural anti-depressant, and also pre-cursors to neurotransmitters such as serotonin, melatonin, dopamine and norepinephrine. It is needed to produce these vital neurotransmitters that keep us happy, optimistic, mentally focused, calm and able to sleep well too. It is the body's primary methyl donor, which does tons of critical stuff.

For some people, the first phase of methyl-folate and B12 production may be ideal, but they have problem producing sufficient SAMe in the body, the crucial methylation pathways will also suffer, resulting in long list of biochemical and physiological disorders. These methyl donors are critical for the completion of both phases to successfully do its job. Please note that methyl-folate gets handed off along with methylcobalamin, which is B12. It’s the body’s number one active form of B12. There’s three of them. To keep it simple, methylcobalamin is number one, most active in circulation. It tag teams with the methylfolate.

Next, we then have genetic variable called MAO-A. Monoamine oxidase A, known as X linked genes, a 'fast-reacting' genes which produces enzymes to clear out or destroy serotonin neurotransmitters in the brain. What that means is women have two genes for MAO, because it’s X. They have two X chromosomes. Men, have an X and a Y. Women can burn through their 5-HTP faster because their MAO-A enzyme, they have twice as much as men. Bear in mind, women typically have twice the amount of these MAO-A enzymes in the body/brain then most men do. What that means is women are more susceptible to depression because that MAO-A is clearing out that 5-HTP faster than the men. Thus, the rate of serotonin depletion in women is much higher then men. Other neurotransmitters such as dopamine may also be depleted in some people with higher amount of MAO-A enzymes. Wonder why more women are suffering from depression compared to men?

Another genetic variable which is CBS genes. It is arguably the number one gene which is associated with high level of homocysteine. If someone has elevated homocysteine, their ability to make neurotransmitters and have them work goes way down. If you have the CBS problem, and that’s a slow down of the gene, same with MTHFR. Now, you must be asking yourself, with all these concerns about possible genes mutation which may increase the susceptibility of depression, where can I get tested? Or what should I do? I have list down couple of websites which provide these specific genetic profile testing and I will be back soon for next post on other variables which can play a role in depression. Stay tuned.

Where can I get tested?
http://moleculartestinglabs.com
https://www.23andme.com



MTHFR, MAO, CBS journals:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1810582/
http://www.ncbi.nlm.nih.gov/pubmed/18370582
http://www.ncbi.nlm.nih.gov/pubmed/26021967
http://www.ncbi.nlm.nih.gov/pubmed/24123968
http://ghr.nlm.nih.gov/gene/MTHFR
http://archpsyc.jamanetwork.com/article.aspx?articleid=207557
http://www.ncbi.nlm.nih.gov/pubmed/25828849
http://www.ncbi.nlm.nih.gov/pubmed/25961058
http://www.ncbi.nlm.nih.gov/pubmed/26028548
http://www.ncbi.nlm.nih.gov/pubmed/24443391
http://www.ncbi.nlm.nih.gov/pubmed/24577139
http://www.ncbi.nlm.nih.gov/pubmed/24091066
http://www.ncbi.nlm.nih.gov/pubmed/25528761