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:


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?

Poll – What impacts your health the most?

What two top things have the most impact on a person's health?

View Results

Loading ... Loading ...


The Brain and SAD (Stress, Anxiety, Depression)

At Baucom Institute, we focus on the needs of the body to function properly like what we eat and how we supplement what we eat.

Over the next several weeks, we’ll be addressing how the brain, its functions and needsdepressed man sitting in the tunnel, are related to SAD – stress, anxiety and depression.

With the medical community using the prescription pad as the answer to helping patients deal with these issues, it’s time to educate the public about the facts and the options to chemical treatment.

First, let’s address the brain and the areas that are affected by SAD:

Amygdala - Part of the limbic system which controls mood, memory and hormone production and actively assigns negative emotions like fear and anger to our thoughts and perceptions; where negative emotional memories are stored and recalled.

Basil Ganglia - Located under the frontal lobes of the brain, the basal ganglia are connected to the frontal lobe cortex which helps movement, thinking, memories and emotions; studies have shown it atrophies with stress, anxiety and depression.

medical  doctor with brain3d meatl in his hands as conceptPrefrontal Cortex - The front most part of the frontal lobe cerebral cortex helps regulate thinking and reasoning, decision-making, and expression of emotions; stress will cause the prefrontal cortex to shut down and actually shrink as well as lessen metabolism.

Hippocampus - Located under the right and left temporal lobes right behind the amygdala, the hippocampus plays a central role in encoding long-term factual memories, works with the amygdala in creating emotional memories; it will reduce in size with chronic stress, anxiety and depression.

Hypothalamus - The nuclei of the hypothalamus will be altered in chronic stress, anxiety and depression which negatively impacts the pituitary master hormones, affecting the functioning of the entire body and brain.

Next time, we’ll address understanding neuron communication and how stress, anxiety and depression affect neurotransmitters.

Have anything to add? We want to hear from you so post below!

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:


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


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.

Autism and Impaired Methylation

  • epigenetics-autism-methylation-baucom-instituteAn increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.

  • Children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione.

  • Consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione).

Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with Autism 1 From the Department of Pediatrics, University of Arkansas for Medical Sciences, and the Arkansas Children‘s Hospital Research Institute, Little Rock, AR (SJJ, SM, and SJ); Niagara Falls, NY (PC); Colden, NY (LJ); Gaylor and Associates, LLC, Eureka Springs, AR (DWG); and Edison, NJ (JAN)2 Rep

PMhx – case:autism-methylation-baucom-institute

  • 6 years old
  • HM hx of severe anxiety,
  • unable to perform in class,
  • crying,
  • restless,
  • insomnia,
  • ADD,
  • dyslexia
  • small bumps on cheeks and upper arms mom describes as acne..

The mother of the child took him to the doctor to medicate him for anxiety and for a referral to a special education program. The mother was considering home schooling due to the severity of the child’s anxiety. This testing was done in addition:

  • Labs:  HLA Dq2/ Hla Dq8 negative

  • Food allergy test + gluten, wheat, dairy, honey, yeast, and some other minor antibodies (leaky gut).

  • MTHFR: c677T+/A1298C+

Stay tuned for the results on our next blog.

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 – Treatment




  • Treatment: 28 day   detox, gluten, diary, soy free, with  protein smoothie (rice) due to low body weight.
  • Di-indole methane and 3 indole-carbinol for estrogen balance, NAC,(glutathione)
  • Trimethyglycine/Methyl -folate & B12 for methylation support
  • L-theanne/Gaba, 5-HTP to improve sleep and pain control
  •  Co-Q10 support
  • Selenium/Lipoic acid,vit E for anti-oxidant support
  • High concentrate EPA/DHA  Magnesium Glycinate 200mg qhs for alkaline, mineral, and bowel support
  • Probiotics, 50 bill/ FOS
  • Exercise daily, check urine ph goal> 6.6.  Sauna at the gym, alkaline diet, Xenoestrogen awareness!

Susan’s response: “I feel the best that I have felt in years. This is miraculous! I sleep deeper than ever, there are no hot flashes, I’m exercising because I have ENERGY, and my husband says I’m back again because I’m SASSY again!”

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?