"What cold medicine do you recommend?" I think I now hear this in my sleep! I 100% recommend THIS cold medicine. I suggest V Clear EPS 7630 to be in every household, there's even a cherry flavor for the kiddos! Prevention is key through diet, lifestyle, and supplements- but sometimes things are out of our control. 

Steer clear of medicines with acetaminophen in them, ​https://www.stittleburgrhc.com/lifestyle-blog/lets-talk-acetaminophen

Please contact Stittleburg Restorative Health Care for more information!
​
Let's get back to health,
Dr. Taryn

​Some quick and easy definitions-

• DNA (deoxyribonucleic acid): Nucleic acid that carried genetic information contained in each cell.
• Genotype: The genetic makeup of an organism.
• Phenotype: The expression of a certain trait based on genetic and environmental influences.

You cannot change your genetic code. The human genome is mostly the same in all people; but there are variations across the genome. A genome is all the genetic material in an organism. A gene is the prime marker of your genetics. Genes are made up of DNA. DNA is passed from parent to child. This is done with the making of new cells, to do this, an existing cell divides in two. Before it divides, the cell copies its DNA. DNA is the hereditary material aka the cells genetic instructions. Sometimes cells make mistakes during the copying process - essentially ‘typos’. These ‘typos’ lead to variations in the DNA sequence at specific locations, called single-nucleotide polymorphisms, or SNPs (pronounced "snips"). Each SNP represents a difference in a single DNA building block, called a nucleotide.

Do you wonder why Brittney from work lost 50 pounds on a specific diet, that you lost 5 pounds on? Do you wonder why your mental/emotional response is significantly different than your parents or your siblings? Do you wonder why your stomach is bloated after eating? Do you wonder why you just can’t get your cholesterol and/or insulin under control? Have you tried “every supplement under the sun” but never noticed any change besides your urine color?

Your DNA is the author of your life- how you process foods, how you detoxify toxins, how you react to environmental stressors, how you react to exercise, how your family health history impacts your health, etc.

These answers can be obtained through a simple cheek swab in our office! SAY WHAT?! Yes, a cheek swab. No poking or prodding trying to find “the good vein.” No long waits in the waiting room. The best part, you can even do this test from home!

This analysis looks at 48 different genes and 61 areas of health to reveal infinite genetic combinations in diet, lifestyle, exercise, sleep, and emotional health.

When it comes to our bodies, making choices that have a positive impact on our health and wellness are vital. The key to your wellness starts (well, started) in your genes! Please contact us today to schedule your free consultation. 

​Let’s get back to health,
Dr. Taryn

"Genes associated with mental emotional health and eating behavior: MTHFR,
FAIM2, MC4R, SEC16B, TMEM18, COMT, NERG1, HTR2A, TAS1R, SLC2A, DRD2,
LEPR:
 Willer, C.J. et al, 2009, Six new loci associated with body mass index highlight a
neuronal influence on body weight regulation. Nature Genetics, 41(1). 25-34
 Morton, L.M. et al, 2006, DRD2 genetic variation in relation to smoking and obesity
in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Pharma
Cogenetics Genomics, 16(12). 901-10
 den Hoed, M. et al, 2009, Postprandial responses in hunger and satiety are
associated with the rs9939609 single nucleotide polymorphism in FTO. American
Journal of Clinical Nutrition, 90(5). 1426-32.
 Doehring A, Kirchhof A, Lotsch J., 2009, Genetic diagnostics of functional variants of
the human dopamine D2 receptor gene. Psychiatric Genetics, 19(5). 259-68
 Furusawa, T.et al, 2010, The Q223R polymorphism in LEPR is associated with obesity
in Pacific Islanders. Human Genetics, 127(3). 287-294

​Genes associated with inflammatory response: ETV5, NCR3, ADIPOQ, GC:
 Chung, H.Y., et al, The inflammation hypothesis of aging: molecular modulation by
calorie restriction. Ann NY Acad Sci 928, 327-335 (2001)
 Ferrucci, L. et al, 2009, Common variation in the beta-carotene 15,15'-
monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide
association study. American Journal of Human Genetics, 84(2). 123-33
 Grimble, R.F., Nutritional modulation of immune function. Proc Nutr Soc 60, 389-397
(2001)
 Grimble R., et al. The ability of fish oil to suppress tumor necrosis factor alpha
production by peripheral blood mononuclear cells in healthy men is associated with
polymorphisms in genes that influence tumor necrosis factor alpha production.
American Journal of Clinical Nutrition. 76(2): 454-459, 2002.
 Terry, c., et al. Cooperative influence of genetic polymorphisms on interleukin 6
transcriptional regulation. Journal of Biological Chemistry. 275: 18138-18144, 2000.
 Morton, L.M. et al, 2006, DRD2 genetic variation in relation to smoking and obesity
in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Pharma
Cogenetics Genomics, 16(12). 901-10.

​Genes Associated with Behavior: MC4R, FAIM2, SEC16B, TAS2R38, DRD2, MTHFR:
 Loos, R.J. et al, 2008, Common variants near MC4R are associated with fat mass,
weight and risk of obesity. Nature Genetics, 40(6). 768-75.
 Willer, C.J. et al , 2009, Six new loci associated with body mass index highlight a
neuronal influence on body weight regulation. Nature Genetics, 41(1). 25-34
 Dotson, C.D. et al, 2010, Variation in the gene TAS2R38 is associated with the eating
behavior disinhibition in Old Order Amish women. Appetite, 54(1). 93-9.
 Vimaleswaran, K. S. et al, 2009, Physical activity attenuates the body mass index
increasing influence of genetic variation in the FTO gene. American Journal Clinical
Nutrition., 90(2). 425-428
 Morton, L.M. et al, 2006, DRD2 genetic variation in relation to smoking and obesity
in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Pharma
Cogenetics Genomics, 16(12). 901-10
 Fushan, A.A. et al, 2009, Allelic polymorphism within the TAS1R3 promoter is
associated with human taste sensitivity to sucrose. Current Biology, 19(15). 1288-
93.
 Matsuo, K. et al, 2006, Alcohol dehydrogenase 2 His47Arg polymorphism influences
drinking habit independently of aldehyde dehydrogenase 2 Glu487Lys polymorphism
Cancer Epidemiology, Biomarkers & Prevention, 15(5). 1009-13

​Genes associated with cholesterol metabolism, triglyceride balance, vascular flow
and tissue development: FTO, ADIPOQ, ETV5, APOA2, LIPC, MTHFR, EDN1:
 Krauss RM, What can the genome tell us about LDL cholesterol? Lancet 2008,
371:450-452.
 Regieli J.J. et al, 2009, PPAR gamma variant influences angiographic outcome and
10-year cardiovascular riski in male symptomatic coronary artery disease patients.
Diabetes Care, 32(5). 839-44
 Bidlack, W. and R. L. Rodriguez, Taylor and Francis , Nutritional Genomics: Dietary
Regulation of Gene Function and Human Disease. 2011.
 Brousseau, M.E., et al, Cholesteryl ester transfer protein TaqI b2b2 Genotype is
associated with higher HDL cholesterol levels and lower risk of coronary heart
disease end points in men with HDL deficiency: Veterans Affairs HDL Cholesterol
Intervention Trial. Arterioscler Thromb Vasc Biol 22, 1148-1154 (2002)
 Rankinen, T. et al, 2007, Effect of endothelin 1 genotype on blood pressure is
dependent on physical activity or fitness levels. Hypertension, 50(6). 1120-5
 Chen, W. et al, Combined effects of endothelial nitric oxide synthase gene
polymorphism (G894T) and insulin resistance status on blood pressure and familial
risk of hypertension in young adults: the Bogalusa Heart Study. Am J Hypertens 14,
1046-1052 (2001)
 Ordovas, J.M. et al, 2002, Dietary fat intake determines the effect of a common
polymorphism in the hepatic lipase gene promoter on high-density lipoprotein
metabolism: evidence of a strong dose effect in this gene-nutrient interaction in the
Framingham
 Dullaart, R.P., et al, Cholesteryl ester transfer protein gene polymorphism is a
determinant of HDL cholesterol and of the lipoprotein response to a lipid-lowering
diet in type 1 diabetes. Diabetes 46, 2082-2087 (1997)
 Verhoeff, B., et al. The effect of a common methylenetetrahydrofolate reductase
mutation on levels of homocysteine, folate, vitamin B12 and on the risk of premature
atherosclerosis. Atherosclerosis. 141(1): 161-166, 1998
 Leeson, C.P., Glu298Asp endothelial nitric oxide synthase gene polymorphism
interacts with environmental and dietary factors to influence endothelial function.
Circ Res 90, 1153-1158 (2002)
 Warodomwichit, D. et al, 2009, The monounsaturated fatty acid intake modulates
the effect of ADIPOQ polymorphisms on obesity. Obesity (Silver Spring), 17(3). 510-
7.
 Brown, C.A., et al, A common polymorphism in methionine synthase reductase
increases risk of premature coronary artery disease. J Cardiovasc Risk 7, 197-200
(2000)
 Corella, D. et al, 2009, APOA2, dietary fat, and body mass index: replication of a
gene-diet interaction in 3 independent populations. Archives of Internal Medicine,
169(20). 1897-906.
 Brown, S., et al. Interaction between the APOC3 gene promoter polymorphisms,
saturated fat intake and plasma lipoproteins. Atherosclerosis. 170: 307-313, 2003.
 Wallace, A., et al. Variants in the cholesterol ester transfer protein and lipoprotein
lipase genes are predictors of plasma cholesterol response to dietary change.
Atherosclerosis. 152: 327-336, 2000.
 Dhillon, P.K., 2011, Common Polymorphisms in the Adiponectin and Its Receptor
Genes, Adiponectin Levels and the Risk of Prostate Cancer. Cancer Epidemiology,
Biomarkers & Prevention, 20. 2618-2627

​Genes associated with antioxidant function, immunity and detoxification: COMT,
NCR3, MTHFR, CYP1A2, ALDH2:
 Rock, C.L., et al, Nutrition genetics and risks of cancer. Annu Rev Public Health 21,
47-64 (2000)
 Pool-Zobul, B, et al, Mechanisms by which vegetable consumption reduces genetic
damage in humans. Cancer Epidemiol. Biomarkers Prev. 7, 891-99 (1998)
 Steinkellner, H., et al, Effects of cruciferous vegetables and their constituents on
drug metabolizing enzymes involved in the bioactivation of DNA-reactive dietary
carcinogens. Mutation Research, 480-481,285-297 (2001)
 Christensen, B., et al, Genetic polymorphisms in methylenetetrahydrofolate
reductase and methionine synthase, folate levels in red blood cells, and risk of neural
tube defects. Am J Med Genet 84, 151-157 (1999)
 Sachae, C. et al, 1999, Functional significance of a C-->A polymorphism in intron 1
of the cytochrome P450 CYP1A2 gene tested with caffeine. British Journal of Clinical
Pharmacology, 47(4). 445-9
 Parke, D.V. “Antioxidants and disease prevention: mechanisms of action”.
Antioxidants in Human Health. CABI Publishing, 1999.
 Chen, J, et al, A methylenetetrahydrofolate reductase polymorphism and the risk of
colorectal cancer. Cancer Res 56, 4862-4864 (1996)
 Jacques, P.F., et al, Relation between folate status, a common mutation in
methylenetetrahydrofolate reductase, and plasma homocysteine concentrations.
Circulation 93, 7-9 (1996)
 Ma, J., et al, Methylenetetrahydrofolate reductase polymorphism, dietary
interactions, and risk of colorectal cancer. Cancer Res 57, 1098-1102 (1997)
 Martinez de Villarreal, L.E., et al, Folate levels and N(5),N(10)-
methylenetetrahydrofolate reductase genotype (MTHFR) in mothers of offspring with
neural tube defects: a case-control study. Arch Med Res 32, 277-282 (2001)
 Slattery, M.L., et al, Methylenetetrahydrofolate reductase, diet, and risk of colon
cancer. Cancer Epidemiol Biomarkers Prev 8, 513-518 (1999)
 Change, A., et al. The effect of 677 C T and 1298 A C mutations on plasma
homocysteine and 5,10- methylenetetrahydrofolate reductase activity in healthy
subjects. British Journal of Nutrition. 83(6): 593-596, 2000.
 Jacques, P., et al. Relation between folate status, a common mutation in
methylenetetrahydrofolate reductase, and plasma homocysteine concentrations.
Circulation. 93(1): 7-9, 1996.
 Miller M., and Mohrenweiser, H. Genetic variability in susceptibility and response to
toxicants. Toxicology Letters. 120(1-3): 269-280, 2001.
 Cosma, G., et al. Relationship between genotype and function of the human CYP1A1
gene. Journal of Toxicology and Environmental Health. 40(2-3): 309-316, 1993.
 Bosron, W. and Ting-Kai, L. Genetic polymorphism of human liver alcohol and
aldehyde dehydrogenases, and their relationship to alcohol metabolism and
alcoholism. Hepatology. 6(3):502 - 510, 1986.
 Takeshita, T. and Morimoto, K. Accumulation of hemoglobin-associated acetaldehyde
with habitual alcohol drinking in the atypical ALDH2 genotype. Alcohol Clinical and
Experimental Research. 24(1): 1-7, 2000.

​Genes associated with glucose balance: DRD2, LEP, PPARg2, PCSK1, LEPR, FTO,
ADIPOQ, PPARD, SLCA2, SH2B1:
 Wilcox G. Insulin and Insulin Resistance. Clinical Biochemist Reviews.
2005;26(2):19-39
 Hautala, A.J. et al, 2007, Peroxisome proliferator-activated receptor-delta
polymorphisms are associated with physical performance and plasma lipids: the
HERITAGE Family Study. American Journal of Physiology Heart and Circulatory
Physiology, 292(5). H2498-505
 Eny, K.M. et al, 2008, Genetic variant in the glucose transporter type 2 is associated
with higher intakes of sugars in two distinct populations. Physiological Genomics,
33(3). 355-60.
 Deeb, S.S., et al, A Pro12Ala substitution in PPARgamma2 associated with decreased
receptor activity, lower body mass index and improved insulin sensitivity. Nat Genet
20, 284-287 (1998)
 Kadowaki, T., et al, The role PPARgamma in high-fat diet-induced obesity and insulin
resistance. J Diabetes Complications 16, 41-45 (2002)
 Li, S., et al. The peroxisome proliferator-activated receptor-gamma2 gene
polymorphism (Pro12Ala) beneficially influences insulin resistance and its tracking
from childhood to adulthood: the Bogalusa Heart Study. Diabetes. 52: 1265-1269,
2003.
 Ostgren, C., et al. Peroxisome proliferator-activated receptor-gammaPro12Ala
polymorphism and the association with blood pressure in type 2 diabetes: Skaraborg
hypertension and diabetes project. Journal of Hypertension. 21: 1657-1662, 2003.

​Genes associated with nutrient utilization: MMAB, KCD10, KCD15, MCM6,
INTERGENIC, BCM01, GC, NBPF3, FUT2:
 • Eastell, R. and Lambert, H., Diet and healthy bones., Calcif Tissue Int 70, 400-404
(2002)
 Lorentzon, M., et al, Vitamin D receptor gene polymorphism is related to bone
density, circulating osteocalcin, and parathyroid hormone in healthy adolescent girls.
J Bone Miner Metab 19, 302-307
 Ralston, S.H., Genetic control of susceptibility to osteoporosis. J Clin Endocrinol
Metab 87, 2460-2466 (2002)
 Prentice, A., The relative contribution of diet and genotype to bone development.
Proc Nutr Soc 60, 45-52 (2001)
 Tanaka, T. et al, 2009, Genome-wide association study of vitamin B6, vitamin B12,
folate, and homocysteine blood concentrations. American Journal of Human Genetics,
84(4). 477-82
 Leung, W.C. et al, 2009, Two common single nucleotide polymorphisms in the gene
encoding beta-carotene 15,15'-monoxygenase alter beta-carotene metabolism in
female volunteers. FASEB J, 23(4). 1041-53
 Wang, T.J. et al, 2010, Common genetic determinants of vitamin D insufficiency: a
genome-wide association study. The Lancet, 376 (9736). 180-188.
 Enattah, N.S.; Sahi, T; Savilahti, E. et al, 2002, Identification of a variant associated
with adult-type hypolactasia. Nature Genetics, 30(1). 233-7
 Ferrari, S., et al, Bone mineral mass and calcium and phosphate metabolism in
young men: relationships with vitamin D receptor allelic polymorphisms. J Clin
Endocrinol Metab 84, 2043-2048 (1999)
 Warren, R.B. et al, 2009, Outcomes of methotrexate therapy for psoriasis and
relationship to genetic polymorphisms. British Journal of Dermatology, 160(2). 438-
41.
 Ferrucci, L. et al, 2009, Common variation in the beta-carotene 15,15'-
monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide
association study. American Journal of Human Genetics, 84(2). 123-33
 Junyent, M. et al, 2009, Novel variants at KCTD10, MVK, and MMAB genes interact
with dietary carbohydrates to modulate HDL-cholesterol concentrations in the
Genetics of Lipid Lowering Drugs and Diet Network Study. American Journal Clinical
Nutrition, 90(3). 686-94"

​*Trauma Trigger Warning* If you or someone you love suffers from depression, lost their battle with depression, attempted to take their life, etc.- this blog may cause immense emotion. 

In the U.S., depression is the leading cause of disability for people over 5 years of age. Did you know, suicide is the SECOND leading cause of death in youth 10-24 years of age in the United States?!

I come from a small town of about 2,000 people, two stoplights, and the world’s largest talking cow- Chatty Belle. A beautiful, intelligent, teenager recently tried to take her own life- she was on an antidepressant at the young age of 14. This truly shook me to my core. I read the statistics, I read the science, I see the mental health crisis every day, I treat mental health every day, but when something so heart wrenching happens so close to home, it’s a different feeling. And it’s something that needs to be spoken about.

Based on the 2017 Youth Risk Behaviors Survey, 7.4% of youth in grades 9-12 reported that they had made at least one suicide attempt in the past 12 months. As a mother, this is terrifying. As a doctor, this is horrifying. As a person, this breaks my heart.

Antidepressant use has increased almost 400% from 1998 through 2008. It’s now the third most common prescription of all age groups. About 60% of Americans have taken antidepressants for more than two years, 14% of them for more than 10 years. If depression is due to a serotonin imbalance that can be “fixed” by SSRIs antidepressants- why are the numbers still increasing? 

This psychiatric hypothesis says that depression results from an imbalance, a deficiency of serotonin at the synaptic level. But this hypothesis is applied to much more than depression. SSRI antidepressants are used to treat a grocery list of problems, like anxiety . (Separate blog on that) 
SSRI antidepressants work in a way of blocking the re-uptake of serotonin.

​When we are led to believe that antidepressants are effective in the short term, it’s very common for patients to remain on these prescriptions for long periods of time sometimes decades.

​“In short, psychiatric drugs induce a pathology. Princeton neuroscientist Barry Jacobs has explicitly made this point about SSRIs .
​​
‘These drugs, he said, alter the level of synaptic transmission beyond the physiologic range achieved under (normal) environmental/biological conditions. Thus, any behavioral or physiologic change produced under these conditions might more appropriately be considered pathologic, rather than reflective of the normal biological role of serotonin.’ (Jacobs, 1991, p. 22)”

​SSRIs disrupt the brain chemistry. E. Fuller Torrey explains, “conditions that disrupt brain chemistry may cause delusions, hallucinations, disordered thinking, and mood swings-the symptoms of insanity" (The Invisible Plague. Torrey, 2001, p. 315) 

“Exposure to Fluoxetine during gestation and lactation affect the DNA methylation of brain and the nociceptive response of rats.” (Behav Brain Res. 2014 May 15;265:142-7. doi: 10.1016/j.bbr.2014.02.031. Epub 2014 Feb 28.)

What does this all mean? Psychiatric drugs disturb normal neurotransmitter function!

While that distress may potentially limit symptoms over short-term, in the long-term it increases the chances that a person will become chronically ill and/or have new or worsening symptoms.
​
“A review of the scientific literature shows quite clearly that it is our drug-based paradigm of care that is fueling this modem-day plague.” Robert Whitaker

What does this mean?! IT MEANS YOU HAVE OPTIONS! Medication is NOT the only option for depression relief. Our children deserve better, we as a society deserve better. I am here to tell you- there is hope. Those of you who are suffering with depression have some great natural, nutritional, and supplemental options.

Depression is a complex symptom. Depression relief must have guidance, please, contact us today to see how we can help!

​I am here to tell you that you are loved, you are enough, and you are needed,
Dr. Taryn

​According to the CDC, in the United States, 16% of women aged 15-44 are currently using the pill. TWO THIRDS of women in the US have used birth control at some point in their life- the pill being the most common form. It’s more important than ever to understand how oral contraceptives can affect a person’s overall health, beginning in the gut.

Now, the pill has significantly reduced the amount of unwanted pregnancies, there is no doubt about that. However, when the pill is readily used for SYMPTOMATIC treatment- this is the issue. 

Birth control was introduced in 1960. What I love about science, it’s always evolving! We know much more now, in 2019, than we did in 1960. Over the years, there has been several studies done on the use of the pill and its effect on inflammatory bowel diseases (IBD), including Crohn’s disease. While each study differs in their focus, methods, and sample size, one common conclusion has been obtained- there is a direct link between oral contraceptive use and your gut

A study in 2016 showed the association between using the pill and cardiovascular disease. If you are a smoker, and take the pill, you have an 80% higher risk of a heart attack. Women that take the pill have 2 times the risk of primary pulmonary embolism and 80% higher risk of hypertension. Oral contraceptive users have a higher risk of invasive breast cancer and were found to be associated with a 2 times higher risk of melanoma. (PMID: 27459451)

Do you suffer from migraines? About 25% of women in the United States do. Did you know that women who take oral contraceptives, and suffer from migraines, have a NINE TIMES HIGHER RISK OF A STROKE?!

Do you suffer from anxiety?! Anxiety is the most common type of mental disorder in the United States. Did you know that with improving your gut microbiome you can help treat your anxiety? In 2019, Yang published a systematic review, published in the Journal of General Psychiatry, stating that “We find that more than half of the studies included showed it was positive to treat anxiety symptoms by regulation of intestinal microbiota.” If you’re taking the pill, it is most likely attributing to your anxiety. ​

Women account for SEVENTY-FIVE PERCENT of ALL auto-immune diseases. Sex hormones in your gut microbiome can affect the development of autoimmune diseases. (PMID: 23328391)

As I previously stated, if you are taking the pill to prevent an unwanted pregnancy, I support your choice. But, let’s talk about the nutrients it’s depleting and be proactive with your health! If you are taking the pill to treat symptoms like irregular periods, acne, PCOS, painful periods, etc.- I am here to tell you that you have other options! And those other options don’t come with a grocery list of potential side effects. Our women deserve better, please, contact us today!

Let's get back to health,
​Dr. Taryn

​Do you toss and turn, with your mind racing, before you finally fall asleep? Do you wake up in the middle of the night, unable to fall back asleep? Do you wake up feeling exhausted?

Why is this?! Drum roll please……. *Stress and Cortisol*

Stress has a profound impact on our stress-coping giant, cortisol. Cortisol is the boss of our stress-response team- which also includes adrenaline and endorphin. Chronic, excessive stress can lead to a permanent hyper-cortisol state. What does that mean? Even after your “stressful events” have passed, your cortisol levels can stay elevated. 

At night, cortisol levels should be at their lowest. When your cortisol levels remain elevated before bed, you sleeping issues ensue. This results in: insomnia, feeling agitated and/or hyper-vigilant, sudden awakening, etc. Chronically elevated cortisol suppresses serotonin and exhausts GABA. 

Serotonin impacts every part of your body. (Read that again) From your emotions to your motor skills- serotonin is vital player. It’s considered the “happy hormone”, because it contributes to overall well-being and happiness.

Fun Fact: about 95% of the serotonin in your body is produced in the lining of your gastrointestinal (GI) tract? Another reason why a healthy gut microbiome is key!

​Now, listed above is a lot of potential symptoms- and is honestly, a little overwhelming. 

At Stittleburg Restorative Health, we utilize an Adrenal Stress Index test that is done from the convenience of your own home- through saliva! That’s right, it can be shipped right to your door and you don’t need to be poked/prodded by a needle. Saliva testing specifically measures free, unbound hormone levels. This eliminates the need to estimate how much circulating hormone is present in a patient’s body.

​The highest form of happiness is health,
Dr. Taryn

I already covered two key factors contributing to autism in https://www.stittleburgrhc.com/lifestyle-blog/lets-talk-autism -the Standard American Diet and the overuse of antibiotics and medications. These two previous key factors can be modified. However, today's topic, you were born with.

This blog is going to be focused on a genetic perspective, specifically the MTHFR gene.
​

​-Severity is based on social communication impairments and restricted, repetitive patterns of behavior-

Over the years there has been a lot of research on autism as we continue to see the rates steadily climb. There are many proposed etiology theories of Autism, ADHD (Attention-Deficit/Hyperactivity Disorder), PDD (Pervasive Developmental Disorder), ASD (Autism Spectrum Disorder), Developmental Disorders, etc:

You cannot change your genetic makeup. The human genome is mostly the same in all people; but there are variations across the genome. A genome is all the genetic material in an organism. DNA is passed from parent to child. This is done with the making of new cells, to do this, an existing cell divides in two. Before it divides, the cell copies its DNA. DNA is the hereditary material aka the cells genetic instructions. Sometimes cells make mistakes during the copying process - essentially ‘typos’. These ‘typos’ lead to variations in the DNA sequence at specific locations, called single nucleotide polymorphisms, or SNPs (pronounced "snips"). Each SNP represents a difference in a single DNA building block, called a nucleotide.

We test for this mutation through saliva or blood. The MTHFR gene provides instructions for making an enzyme called methylenetetrahydrofolate reductase. (So, the MTHFR gene produces the MTHFR enzyme.)

• MTHFR is responsible for converting folate into its active state.
  • It helps convert an inactive form of folate into the active form of folate which then gets pushed forward through the cycle to be able to generate methyl donors, to be able to support the detoxification processes, to be able to support neurotransmitter production, to be able to support choline... Which choline is vitally important to neural health. MTHFR is kingpin to many different bodily processes.
• It is an irreversible process and is the rate limiting enzyme in this pathway

​Before I talk about certain locations of SNPs, I want to explain that these numbers most likely mean nothing to you.  However, they are very important and useful to me. Just like shelving a book in the library, the librarian knows exactly what the important, random combination of letters and numbers are used for- think of me as the librarian on your genes. 

The two different places that we look at for MTHFR deficiencies are locations 677 and 1298. The SNPs of MTHFR affect how well the body is able to activate folate into the bioactive form. Through Functional Medicine, these mutations can be found and treated with supplementation, diet, and lifestyle.

​Get this! An analysis performed at a Portland, OR based lab showed that roughly 86% of symptomatic patients have at least one MTHFR polymorphism. What does that mean? Almost 9 out of every 10 patients with autistic or other neurological symptoms, probably have at least one MTHFR polymorphism that is affecting their ability to generate active folate.

MTHFR in general has been associated with increased ASD risk.

​MTHFR C677T is associated with the greatest influence on enzyme activity and increased overall ASD risk.

MTHFR 677 is more present in autism.

MTHFR A1298C has been reported to have a more influential effect on mental health disorders.

So, what does this all have in common?! NEUROTRANSMITTERS. Neurotransmitters are our body’s chemical messengers i.e. very important. 

Now, this was a lot of science and a lot of information. I am here to educate, inform, and spread awareness and hope. The mutations and pathways I mentioned above CAN be supported with certain supplements and diet/lifestyle changes. NEVER let anyone tell you that you must just accept your illness and learn to live with it. If you would like information on how Functional Medicine can help autism, please contact Stittleburg Restorative Health Care!

Let's get back to health,
​Dr. Taryn