SAD – How Emotions Drive Stress, Anxiety and Depression

In the last blog, we looked at the chemical reaction in our brains, specifically with three of the 50+ communicating chemicals called “neuroamines” – either too much or too little can lead to either end of the spectrum of emotional issues i.e. panic attacks, depression, etc.

In this blog, we will go into more detail on how emotions drive us to stress, anxiety and depression. We have what are called “Three Brains” – the cerebral cortex, the limbic system and the brain stem. Here’s the process of how these three interact and produce the chemical reaction with emotions:

Thinking

Cerebral Cortex – the front lines where information is taken in. When we experience or perceive something, we think about it.

Limbic – When our thoughts are produced, they are then sent to this system where the hippocampus assigns any memories we have of this experience/perception and the amygdala help assigns an emotion to that thought.

Brain Stem – When an emotion is assigned, the brain stem then regulates the body’s response to that emotion.

What emotions do you struggle with?

SAD (Stress, Anxiety and Depression) and Understanding Neuron Communication

There’s nothing more complicated than emotions – sadness, stress, anxiety, depression. How do you control them? How do you deal with them? How do you keep these emotions from negatively affecting you?

Research is ongoing but more has been done to find the link between our brain, emotions and how healthy we are.serotonin-neurons-baucominstitute-stress-anxiety-depression-blog

One way to approach this complicated connection is to understand how it all works.

There are as many as 40-50 different chemicals in the brain, spinal cord and peripheral nerves that serve as neurotransmitters. These neurotransmitter molecules quickly travel the synapse to lock into protein receptor sites. When enough neurotransmitters are locked in to the receptors there is an electrical charge that is activated.

In the case of emotions and mental incapacities, these neurotransmitter mechanisms can go awry and the interactions between the neurons can become overactive or underactive. Both overactivity and underactivity can cause problems. Abnormal levels of serotonin, norepinephrine, dopamine, glutamate and gamma-aminobutyric acid (GABA) are found in chronic stress, anxiety and depression.

When someone goes to the doctor and receives medication for one of these issues, the doctor is hoping to re-adjust the levels of various neurotransmitters in the brain that are out of balance.

SAD-stress-anxiety-depressionFor example, Prozac or some other antidepressant will be prescribed for depression where as Gabapentin or Neurontin will be prescribed for anxiety.

Where the rubber meets the road, specifically, is with three of the 50-odd brain chemicals called “neuroamines” – serotonin, norepinephirine, and dopamine. These chemicals are produced primarily in the brain stem and circulate throughout the brain. Abnormalities in these chemicals lead to pervasively high levels of two basic emotions: fear and sadness, which are driving forces behind stress and fear. For example, elevated levels of norepinephrine are associated with chronic stress and anxiety disorders including panic attacks and phobias. Decreased levels of serotonin, norepinephrine and dopamine are thought to be involved with depression.

We’ll break this down more next blog and how emotions are the driving force that create SAD – stress, anxiety and depression.

What is a takeaway that helps you from this blog?

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Methylation and Nutrition

We’ve been on a long series about Methylation and how an individual’s nutrition can affect the outcome of their health. Here’s a quick review of MTHFR:

MTHFR-baucom-institute

Once the MTHFR tests shows (+) variants exist, what else can the health provider do to effectively treat the patient?

MTHFR-solutions-baucom-institute

So, what are you doing as a patient to take control of your health in relation to genome testing and restorative care with a physician that understands the impact of these aspects?

As a medical practitioner, are you having your patients tested for this all important genome so that they can be more proactive with their health and prevent disease?

Autism and Impaired Methylation: PMhx Case – Chris

From the last blog we presented impaired methylation and the connection to autism. This week, we look at a specific case where a subject, named Chris, was given treatment through nutrition and supplements.

  • Treatment: Elimination diet 6 weeks followed by no gluten or cow dairy.autism-baucom-institute

  • EPA/DHA liquid

  • chewable muti-vitamins (organic)

  • Probiotics c FOS

  • B12/5mthf, B6, mg glycinate, Nac

  • Phospho serine at  Hs

The symptoms resolved! Although a few minor issues with dyslexia continued, Chris integrated back into school after his mom took him out of school and home schooled him for a year until she could control his diet.  Methyl-folate and methyl-B12 were added this past year which helps energy and support detoxification in Phase II of the liver function.

nutrition-autism-baucom-instituteINTERVENTION 1: Supplementation with folinic acid and betaine

Although supplementation was effective in normalizing the methionine cycle metabolites to the concentrations in the control subjects, the intervention significantly improved but did not normalize tGSH or GSSG concentrations or tGSH:GSSG

INTERVENTION 2: Supplementation with folinic acid and betaine and Methyl vitamin B12

The addition of injectible methylcobalamin (intervention 2) did not alter the mean concentrations of methionine, SAM, SAH, or homocysteine beyond the alterations induced by the intervention with folinic acid and betaine. However, relative to intervention 1, the addition of injectible methylcobalamin further decreased the concentrations of adenosine and GSSG and further increased the concentrations of methionine, cysteine, and tGSH and SAM:SAH and tGSH:GSSG.

Xenobiotic Effects on COMT

A xenobiotic is a foreign chemical substance found within an organism that is not normally, naturally produced by or expected to be present within that organism. It can also cover substances which are present in much higher concentrations than are usual.41_SchemaRTS_Eng

  • In humans, 2-Oh and 4-Ohestradiol (catechol estrogens) are rapidly O-methylated to form monomethyl ethers catalyzed by COMT and S-adenosyl-L-methionine.

  • Xenobiotics may strongly inhibit COMT-mediated
    O-methylation of catechol estrogens by xenobiotics and may facilitate the development of estrogen-induced tumors.

  • Xenobiotics may therefore deplete intermediates in the Folate cycle.  Environmental burden of Xenobiotics may create a higher need for methylation support.

Catechol-O-methyl_transferase_baucom-instituteAbstract: COMT genotype, micronutrients in the folate metabolic pathway and breast cancer risk - Goodman JE, Lavigne JA, Wu K, Helzlsouer KJ, Strickland PT, Selhub J, Yager JD; Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD 21205, USA.

  • Catechol-O-methyltransferase (COMT) catalyzes the O-methylation of catechol estrogens (CEs), using S-adenosylmethionine (SAM) as a methyl donor.

  • Several studies have indicated that the val108met COMT polymorphism, which results in a 3-4-fold decrease in activity, is associated with increased breast cancer risk.

  • Folate, whose intake levels have also been associated with breast cancer risk, and other micronutrients in the folate metabolic pathway influence levels of SAM and S-adenosylhomocysteine (SAH), a COMT inhibitor generated by the demethylation of SAM.

  • Because these micronutrients have been shown to alter SAM and SAH levels, we hypothesized that they could also affect COMT-catalyzed CE methylation.

  • Although measurements of SAM and SAH were not initially collected, a secondary analysis of data from two nested case-control studies was performed to examine whether serum levels of folate, vitamin B12 (B12), pyridoxal 5′-phosphate (PLP), cysteine and homocysteine, in conjunction with COMT genotype, were associated with breast cancer risk. COMT(HH) (high activity COMT homozygote) breast cancer cases had statistically significantly lower levels of homocysteine (P = 0.05) and cysteine (P = 0.04) and higher levels of PLP (P = 0.02) than COMT(HH) controls. In contrast, COMT(LL) (low activity COMT homozygote) cases had higher levels of homocysteine than COMT(LL) controls (P = 0.05).

  • No associations were seen between B12, COMT genotype, and breast cancer risk. An increasing number of COMT(L) alleles was significantly associated with increased breast cancer risk in women with below median levels of folate (P(trend) = 0.05) or above median levels of homocysteine (P(trend) = 0.02). These findings are consistent with a role for certain folate pathway micronutrients in mediating the association between COMT genotype and breast cancer risk.

These findings are consistent with a role for certain folate pathway micronutrients in mediating the association between COMT genotype and breast cancer risk.

Case Study: Susan

  • 49 yo CF recent dx of Stage II Breast Ca hormone Rec +,s/p partial mastectomy, body-case-study-baucom-instituteradiation, irregular periods, shingles, intolerant of Fereston due to Headaches, constipated.  Hx of fibroids, heavy periods, fibrocystic breast. G2P2

  • nl vitals,   Estradiol 26.8pg/ml (0-32.2 menopause range)

  • Sed rate 22 (0-20)

  • Cbc, chem, thyroid panel cholesterol wnl

  • Vit D 153 (30-100)

  • GGT 15   Uric Acid 3.2

  • Glutathione 992

  • MTHFR C677+/A1298C+

  • Cytokine: base Il-6++, IL-17+, IL-12–,IFN gamma ++, TNF-a ++, IL-4++, IL-5–, IL-10++, IL-8++, G-CSF++

How would you approach treatment of this patient?

Spectracell-Methylation-Susan-Baucom-Institute

Catechol-O-Methyltransferase

Spectracell Methylation Presentation.pptx

 

  • Involved in phase II metabolism of hydroxy-estradiols
  • Involved in metabolism of xenobiotics
  • Involved in metabolism of chocolate
  • Involved in metabolism of caffeine by-products (catechins)
  • Involved in metabolism of excitatory neurotransmitters

Spectracell Methylation Presentation.pptx (1)

  • S-adenosylmethionine and magnesium dependent
  • Linked to estrogen
  • imbalance disorders
  • Is involved in hyperhomocystinemia in Parkinson patients on L-dopa
  • Is linked to psychiatric disorders

Spectracell Methylation Presentation.pptx (2)

Methionine Synthase Mutations

  • 250px-PBB_Protein_MTR_image_Baucom_InstituteMutations in the MTR gene have been identified as the underlying cause of methylcobalamine deficiency.

  • This may lead to megaloblastic anemia as seen in elevated MCV in the patients CBC.

  • Patients may actually have high levels of B12 in the serum as the Cobalamine is not converting to Methylcobalamine.

  • May compound mutations in MTHFR

Mega Dosages of Me-B12B12_b-s

  • Supplementation with megadoses of MeB12 has been advocated to protect the cognitive function of patients suffering from:

  • Chronic Fatigue

  • Stroke

  • Depression

  • Alzheimer’s disease Neurological diseases

Folate Cycle Nutrients, Homocysteine, and Transsulfuration

  • Transsulfuration is the conversion of Homocysteine with the co-factors B6 and Serine to Cystathionine.

Homocysteine-Damage-Ladd-McNamara

  • Cystathionine is then converted to Cysteine which is one of the three amino acids that compose Glutathione.
  • Polymorphisms in Cysta beta-synthase may affect the rate of conversion of Cystathionine to Cysteine.
  • Cysteine is thought to be the rate limiting step in the formation of Glutathione.

glutathione-structure-baucom-institute (2)