The role of thiamine and diet in the development of Autism Spectrum Disorders

1. Lucine Health Sciences, Inc. | Hormones Matter
Thiamine Deficiency
Disease
Dysautonomia, and High Calorie
Malnutrition Calorie Malnutrition

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Introduction
Who, what and why.

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Authors
Derrick Lonsdale, MD, FACN, CNS,
retired
• Cleveland Clinic, Pediatrics 20 years
• Head of Biochemical Genetics
• Private practice 20 years specializing
in nutrient-based therapy.
• Over 100 published papers in medical
journals
• 68 articles on Hormones Matter

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Authors
Chandler Marrs, MS, MA, PhD
• Independent research scientist, writer, women’s
health, mitochondria
• Neuroendocrinology, maternal health
• Academic articles on maternal health
• Lucine Health Sciences, Hormones Matter
• Medication/vaccine adverse reactions
research
• 250 articles published on Hormones Matter
• Micronutrient Deficiencies and Mitochondrial
Dysfunction. In Integrative Therapies for
Depression. J Greenblatt and K Brogan, Eds.

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What I Do Officially

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What I Really Do
o150,000+ monthly
views
o1200+ articles and
growing
o150 guest
contributors/writers
• 18 PhDs, 5 MDs, 2
DPTs
oThousands of
comments
Cause trouble.

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Listen and learn

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And try to untangle
The untanglible.

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What I have learned
oEnvironment matters
• Perhaps more than genetics
oHealth and disease are both sudden and slow
• Thresholds and tipping points
oAll about the mitochondria
• Mitochondria determine everything
• At nexus of disease and health
• Cause and consequence
And thiamine is really that important.

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Thiamine and Mitochondrial
Function
An indissoluble relationship

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What is thiamine?
oVitamin B1 (thiamin, thiamine) found in
• Lean pork, poultry and other meats, wheat germ, liver and
other organ meats, eggs, fish, beans, peas, nuts, whole grains,
garlic.
oAntagonized by
• High carbohydrate/sugar diets, coffee, tea, betel nuts, raw fish
• Many (all) pharmaceutical, environmental, and industrial
chemicals
oCritical for
• Mitochondrial energy production, protein expression, and
general function, and array of CNS/PNS functions

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Why is thiamine important
oCofactor for multiple enzymes involved in
mitochondrial energetics
• Transketolase
• Pyruvate dehydrogenase complex (PDC)
• Lactate dehydrogenase (LDH)
• Alpha ketoglutarate dehydrogenase (a-KDH)
• Branched-chain alpha-keto acid dehydrogenase (BCKDH)
• Alpha oxidation in peroxisomes (HACL1)
oOften works together with other co-factors
• Magnesium
• Riboflavin (B2)
• Alpha lipoic acid (ALA)
Without thiamine,
mitochondrial respiration
grinds to a halt.

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Thiamine is critical for ATP
production
And ATP is critical for life.

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Thiamine and hypoxia
oMolecular oxygen consumption
• Whether and how effectively blood oxygenation
occurs depends upon vitamins and minerals
• Hypoxia absent obstruction
HIF signals ~100 other proteins involved in: angiogenesis, erythropoiesis,
iron and glucose metabolism, growth factors and apoptosis.

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An aside: HIF and women’s
health
Endometriosis and Heavy Menstrual
Bleeding: Two Sides of the Same Molecular
Coin
• Endometriosis
• HIF controls spread of endometriotic
lesions
• Invasion into other tissue
• HIF supra-elevated
• Heavy menstrual bleeding
• Decreased HIF
• Both involve mitochondrial survival cascades

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Thiamine regulates protein
expression
oSuccinate thiokinase forms forms a multienzyme complex
with the alpha-ketoglutarate catalyzes succinyl-
CoA>succinate
oSuccinate dehydrogenase oxidizes succinate to fumarate
and uses the electrons generate to catalyze reduction of
ubiquinone to ubiquinol for complex II (TCA>ETC linkage)
o20% ↓ Malate dehydrogenase = ↓ ATP from 38 to ~13 units
(in culture)
o↓ Pyridoxal kinase: dietary vitamin B6 into the active
cofactor form pyridoxal 5′-phosphate (PLP)

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Thiamine insufficiency or
deficiency
oReduced ATP
• Reduced cellular energy: spotty energetics
• Reduced oxygenation – chronic, low level
hypoxia
• Mitochondrial dysfunction, apoptosis and
necrosis
• Misfolded proteins
oIncreased compensatory survival signals
• HIF
• Inflammation
• ROS
• Mitochondrial death spiral
Reduced ability to
meet
bioenergetic
demands of
everyday
stressors

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Traveling PDC Enzyme

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If thiamine is that important
Why don’t we monitor it?

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If we think of thiamine deficiency
oWe think of late stage, frank deficiency in specific populations
with purely neurological symptoms
• Wernicke’s encephalopathy in chronic alcoholics
• Ataxia, nystagmus, confusion/memory loss
oWe miss the earlier symptoms in this and other populations
• And we mostly miss Wernicke’s too
• 80% of alcohol related Wernicke’s missed 1
• 58% of pediatric Wernicke’s missed2
• Unknown % of hyperemesis gravidarum Wernicke’s missed
• Only 16% cases exhibit classic triad1
1. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):341-5.; 2. Pediatr Neurol. 1999 Apr;20(4):289-94.

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Lonsdale & Marrs, 2017

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We don’t consider the broader
population
o76% of diabetics (type 1 and type 2)
o29% of obese patients, 49% post bariatric surgery
o40% of community dwelling elderly, 48% of elderly
patients in acute care
o55% of cancer patients
o20% ER patients (random sample, UK)
o33% congestive heart failure patients
o38% pregnant women, more with hyperemesis
o30% psychiatric patients
Lonsdale & Marrs, 2017

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Partly because
oWe fail to recognize
• More subtle, metabolic disturbances
• Mitochondria regulate metabolism. Starve the mitochondria
of thiamine, alter metabolism.
o Phenotypically distinct
• Non-linear, but chronic time course of symptom
development
o Symptoms wax and wane before reaching critical point
• That there is a problem
• We solved nutrient deficiency, didn’t we?

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Reframing nutritional
considerations
Industrial food production and high calorie malnutrition

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Why don’t we consider thiamine
in clinical care?
“Only a small percentage of the population had total
usual intakes (from dietary intakes and supplements)
below the estimated average requirement (EAR) for
the following: vitamin B-6 (8%), folate (8%), zinc (8%),
thiamin, riboflavin, niacin, vitamin B-12, phosphorus,
iron, copper, and selenium (<6% for all).”
We think thiamine deficiency is rare.

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Fortification programs solve
nutrient deficiencies
“Fortification contributed greatly to intakes of many
micronutrients, reducing the percentage of the population having
intakes belowthe Estimated Average Requirement (EAR)
without adding appreciably to the percentage having intakes
above the Upper Tolerable Intake Level (UL).”
Or do they?

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If we dig a little deeper
“Without added nutrients, a high percentage of all
children/adolescents had inadequate intakes of
numerous micronutrients…”

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Where fortification and
enrichment come into play
High calorie malnutrition

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Junk food and nutrient
sufficiency?
An oxymoron.

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Dietary assumptions
oImpact how we view
• Food and nutrition in general
• Food and poverty
oFrame conversations and research on
mitochondrial functioning
• Calories in, ATP out
• Calorie restriction = mitochondrial health

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Unpacking dietary assumptions
oCalorie insufficiency sole determinant of
malnutrition
• So long as there are sufficient calories malnutrition
is rare
oEmpty calories plus enrichment and/or
fortification provide nutrient sufficiency
• Up to a point, this may be true
oIndustrial foods are equivalent to ‘real’ food

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On the one hand
oPoverty and subsistence level malnutrition in
non-western countries
• Limited absolute calories
• Fortification postpones outright malnutrition
oPoverty and subsistence level malnutrition in
western countries
• Adequate or excess calories
• Processed foods are cheaper than real food
• Fortification postpones and disguises outright
malnutrition

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For example:
o Autism rates for each state compared to infant
nutrition
• Duration of exclusive breast-feeding
• Participation in WIC program
• Infant nutrient levels
oAssociations between
• ↑ WIC =↓ autism
• ↑Breastfeeding (by nutrient starved moms) = ↑infant
nutrient deficiency + ↑ autism rates
J Am Coll Nutr. 2011 Oct;30(5):348-53.

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Similarly
oThiamine fortified foods prevent frank deficiency in
non-western countries with food scarcity

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On the other hand
oFood abundance and high calorie malnutrition
• Partly from excess calories (3500 kcal daily)
• 1.9 billion adults are overweight
• 41 million children <5 years
• 30-40% of Americans
• Partly from industrial farming and agriculture
• Even healthy food is devoid of nutrients
oCalories and fortification disguise malnutrition
• Thiamine dependent enzymes cannot meet the processing
demands of high calorie, carbohydrate dense diets
o Cannot converted ingested thiamine into TPP

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Global Report on Nutrition
oMalnutrition is alive and well, even in first
world countries
…multiple interleaving forms of malnutrition ranging
from child and adult micronutrient insufficiency to
obesity.
International Food Policy Research Institute. 2014. Global
Nutrition Report 2014: Actions and Accountability to
Accelerate the World’s Progress on Nutrition. Washington,
DC.

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Digging a little bit deeper
oConventional agriculture
• Pesticide/herbicide drenched produce genetically
modified to withstand the toxins1
• Limited genomic diversity2
• 70% of world’s diet comes from 15 crops
• Cultivated out 95% of ~200,000 plant metabolites
oMineral depleted soils
• ~85% reduction in US and Canada3
1. 2. Daniell & Ryan 2012. DOI: 10.5772/33500; 3. Marler & Wallin, 2006. http://www.nutritionsecurity.org/PDF/NSI_White%20Paper_Web.pdf

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Conventionally grown produce
oCarries high toxic load
• Glyphosate plus adjuvants1,2
• Chelate minerals,
• Blocks glycine (analog)
• Alters vitamin A metabolism
• Destroys gut bacteria
• Damages mitochondria (ETC I, III), reducing ATP by 40%
• Endocrine and nervous system disruptor
oContains ~40 % fewer nutrients than the same foods 50
years ago3
oHigher in sugar content4
1. Serralini et. al., Seneff et al. 3. Bull Environ Contam Toxicol. 1979 Jun;22(3):357-64. 4. Daniel & Ryan, 2012, The
nutrigenome and gut microbiome: chronic disease prevention in crop phytochemical diversity.

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Industrial meat production
oRaised in unsanitary
conditions
oHeavy use of
antibiotics and
hormones
• 85% of world’s
antibiotics
oPoor feed quality
oHigher chemical load
• EDCs banned
elsewhere permitted
here
oHigher saturated fat
content
oLower micronutrient
content
Lonsadle & Marrs 2017

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High calorie malnutrition
oPoor food quality
• All sorts of nutrient
deficiencies
oMismatch between
caloric and nutrient
intake

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Restricted diet and thiamine
deficiency

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What else causes thiamine
deficiency
• Alcoholism
• Current and familial
• A sweet and high-carbohydrate food-liking pattern
was 48% heritable

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Thiamine deficiency
• Bariatric surgery
• Absorption of thiamine occurs in small intestine
• Parenteral nutrition
• Gut dysbiosis: both cause and consequence
• Candida overgrowth, SIBO, trehalose (↑
microbial virulence)

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Pharmaceutical, environmental, and
industrial chemicals damage the
mitochondria and/or deplete nutrients by
one mechanism or another.
Toxicol Sci. 2013 Jul;134(1):1-17. doi: 10.1093/toxsci/kft102. Epub 2013 Apr 29. ; Am J Physiol Cell Physiol. 2007 Jul;293(1):C12-21. Epub 2007
May 2.; Mol Interv. 2010 Apr;10(2):98-111. doi: 10.1124/mi.10.2.7; J Child Neurol. 2014 Sep;29(9):1241-8. doi: 10.1177/0883073814538510.
Epub 2014 Jul 9.
Poor nutrition and high toxic load: a recipe for disaster.

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Genetic factors: transporters
oGenetic/epigenetic alterations in transporters
• Solute Carriers (SLC): 395, 52 families
• SLC19A1: folate, but thiamine mono- and di- phospho
derivatives are substrates for SLC19A1
• SLC19A2 (ThTr1): systemic thiamine transport –TRMA, most
highly expressed in muscle
• SLC19A3: (ThTr2): intestinal thiamine absorption – biotin
responsive basal ganglia disease
• SLC25A19: mitochondrial TPP carrier –Amish microcephaly
• SLC35F3: thiamine, hypertension
https://doi.org/10.1016/j.bbabio.2017.03.006; Mol Aspects Med. 2013 Apr-Jun; 34(0):
10.1016/j.mam.2012.07.006. doi: 10.1016/j.mam.2012.07.006; J Am Coll Cardiol. 2014 Apr 22;63(15):1542-
55. doi: 10.1016/j.jacc.2014.01.007.
SNPs
common in
individuals
with chronic
illness and
medication
reactions

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Enzyme activity
Plasma thiamine, thiamine
monophosphate similar in ASD
children and controls but TPP 24%
lower in ASD group, suggesting
problem absorbing, metabolizing
thiamine.

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Ann Neurol. 2017
Sep;82(3):317-330. doi:
10.1002/ana.24998. Epub
2017 Aug 30.

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20-50% of the population
One crisis away from overt thiamine
deficiency
Who is thiamine vulnerable?

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“There is often something sinister about familiar concepts.
The more familiar or ‘natural’ they appear, the less we
wonder what they mean; but because they are widespread
and well-known, we tend to act as if we know what we
mean when we use them.”
Devisch, I. & Murray, S., 2009. doi:10.1111/j.1365-2753.2009.01232.x
Rethinking nutrient adequacy
Maybe we haven’t solved nutrient deficiency after all.

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Revisiting mitochondrial
energetics
Beyond the black box

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Mitochondria
Energy

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So long as there are sufficient
calories (macronutrients)
We get ATP.

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All this happens magically

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“The presumption is that all calories are created equally
e.g. that calories are calories and no matter the origins of
those calories, the end result will be ATP. Indeed, from the
mitochondrial perspective, each fuel, no matter its origins,
will be broken down to its carbon skeleton and through a
series of reactions, the final output will be ATP. In that sense,
the fuel source makes little difference: the net result will be
ATP.”
Lonsdale & Marrs, 2017

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“However, and this is a big however, what this perspective
fails to recognize, is to get from fats, proteins and
carbohydrates to ATP, there is an entire
factory of enzymatic reactions that absolutely require non-
caloric nutrients - vitamins and minerals – to function
properly.”
Thiamine is top among them.
Lonsdale & Marrs, 2017

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More than just calories
22 vitamins
and minerals

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While all the nutrients are important…
• Thiamine is the
gatekeeper.
• Transketolase
• PDC
• LDH
• HACL1
• Sitting atop, at the entry
points for processing
pathways

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TPP

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TPP
↓ATP
Functional
changes in the
mitochondria
Altered
chemistry

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When the mitochondria lag
oHigh energy organ systems impacted most
dramatically
• Nervous system
• Cardiovascular system
• Gastrointestinal
• Musculature
oMetabolic changes locally <> systemically

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Spotty energy: autonomic
instability

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Biochemistry for Medics: http://www.slideshare.net/namarta28/thiamin

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• Fatigue, exercise intolerance, decreased
wakefulness (orexin/hypocretin)
• Cyclic vomiting , gastroparesis and pseudo
bowel obstructions
• Myalgia, myopathy, neuropathy
• Migraines, seizures, syncope
• Ataxia and tremors
• Hormone disorders
• Depression, mania, anxiety, psychosis
• Cognitive impairment
• Diabetes, metabolic, inflammatory and
immune dysfunction
Symptomatically
General autonomic
instability, affecting
everything that the
ANS regulates

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“…Mitochondrial dysfunction doesn’t really cause anything,
what it does is predisposes towards seemingly everything.
It’s one of many risk factors in multifactorial disease. It can
predispose towards epilepsy, chronic fatigue, and even
autism, but it doesn’t do it alone. It does it in combination
with other factors…
it predisposes for disease throughout the entire system.”
Dr. Richard Boles, Geneticist

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Mitochondria at the nexus of
health and disease by design

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From the lab to the clinic
Induced and expressed thiamine deficiency

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Thiamine deficiency
o 3 groups of female rats: Ad lib, thiamine supplemented,
thiamine deprived (TD)
oTD group
• 2.5 weeks:
• weight loss, anorexia, hair loss, drowsiness, no neurological signs
• 4.5 weeks: rapid progression of symptoms, decline of health
over next 5 days
• incoordination with walking, impairment of the righting reflex,
reluctance to walk, walking backwards in circles, imbalance, rigid
posturing and eventually a total loss of righting activity and severe
drowsiness
• Thiamine injection corrected within 24 hours
J Clin Invest. 1968 Oct; 47(10): 2268–2280.
doi: 10.1172/JCI105912

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Threshold effect
o Brain thiamine across time
• Neurological symptoms apparent when cerebral
thiamine concentrations reach 20% of normal.
• 80% thiamine depletion before recognizable
neurological symptoms develop
• Recovery begins when concentrations climb to
26% of normal.
• 6% over depletion state improves function
J Clin Invest. 1968 Oct; 47(10): 2268–2280.
doi: 10.1172/JCI105912

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Maternal TD and brain development
oTime dependent, process and region specific
disturbances of neuronal development
• Reduced hippocampal neuronal density (nd) and size (s)
• Prenatal TD: 39.67%nd, 7.97%s (Dentate gyrus, CA4)
• Perinatal TD: 26.75%nd, 12.95%s (Dentate gyrus, CA4)
• Postnatal TD: 14.2%nd, 10.77s (CA1)
• Perinatal TD: cell differentiation
• Postnatal TD: axon, dendrite growth, synaptogenesis
and myelinogenesis
Acta Neurobiol Exp (Wars). 2005;65(4):387-98.

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TD in infancy: the Israeli experience
oOctober – November 2003 infants hospitalized with
encephalopathy symptoms included:
• Lethargy, vomiting, constipation, nystagmus, seizures,
coma
oSoy based formula without thiamine fed to 600-
1000 infants
• ~20 infants hospitalized
• 3 died acutely, 1 died after 6 year vegetative state
• 10 severely developmentally delayed, epilepsy and other
disorders

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Israeli experience continued
o20 infants exposed to TD formula initially
considered non-neurologically affected re-
evaluated at 3 years
• Initial presenting symptoms: lethargy, irritability,
constipation, vomiting
o~ 50% had developmental delays
• Language and motor development
• Moderate to severe
Brain. 2011 Jun;134(Pt 6):1720-39. doi: 10.1093/brain/awr068. Epub 2011 May 9.

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Primary vs secondary TD
Ann Neurol. 2017
Sep;82(3):317-330. doi:
10.1002/ana.24998. Epub
2017 Aug 30.

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Time course of symptoms
oEarly/mild TD
• Sleeping, fatigue, anorexia, depressed mood, reduced activity, apathy,
parasthesias, muscle pain, dizziness, cognitive fuzziness.
o Moderate/prolonged, without caloric restriction
• Compensatory reactions (lactate and inflammation), instability becomes a
cardinal feature.
• Mitochondria are increasingly incapable of meeting energy demands and minor
stressors initiate symptoms.
• Mood lability, irritability, fearfulness progressing to agitation, cognitive impairment, and
difficulty finding words, comprehending text and memory issues become more
prominent. Depending upon the patient, GI dysmotility symptoms such as gastroparesis,
excessive vomiting, diarrhea and/or bowel irritability might emerge, along with
neuropathic pain and ataxias, tremors and syncope; cardiac instability, palpitations,
precordial distress on exertion (pseudoangina), insomnia, anorexia, nausea, vomiting,
weight loss, hypotension, bradycardia at rest, and tachycardia with sinus arrhythmia on
exertion

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Non-linearity of expression
Stressors evoke symptoms.

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Low thiamine, elevated B9 and
B12

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Thiamine and ASD
o Small pilot study – 10 children
• TKA and TPPE pre and post
• Pre, 30 days, 60 days urinary measures of SH-reactive metals,
total protein, sulfate, sulfite, thiosulfate and thiocyanate; hair
analysis
• Autism Treatment Evaluation Checklist (ATEC) forms
• Treated TTFD 50mg 2X per/day rectally 60 days
• At baseline, 3 showed TD, 6 high arsenic, 10 traces of
mercury
• Results: 8 improved ATEC, arsenic decreased, but variable
increase excretion of other metals

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Treatment

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Take home
oNutrients matter, thiamine a bit more than
others
• Two questions to ask in clinical care
• What nutrients does the patient need for health?
• Is he/she getting them?
• And perhaps a third question
• Is the toxic load too high for mitochondria to clear?

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Mind your mitochondria.
Feed them well and life will be good.

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Understanding Mitochondrial Nutrients
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