Reflections on Autism
A number of you have asked me about autism and Asperger’s Syndrome and what you might do nutritionally. While I am not an expert in autism, I can outline some of the research that is being done and share my reflections on how it might fit together. You have the lived experience. Perhaps we can explore our way to some working solutions.
I have often wondered about autism. A couple of years ago I got a gorgeous rescue golden retriever. Her people gave her up because she was a “behavioral problem”. I took her and then observed. She would not connect, made no eye contact, and spent her days immobile with her head under the bed. She collected all the dog toys and hoarded them with her there under the bed. She could not cope with new experiences. She was stubborn, willful and terrified of rain and thunder. I worked with her behaviorally for 6 months with no change made.
Eventually, I took her to a homeopathic vet to see if he might offer some perspective. We met for an hour. He said, “I think she is autistic.” He had a remedy for her, but had to order it and said it would take 2 weeks. I figured while I was waiting, I would play with her food and see what happened. I did and in 3 days, this dog was transformed. She connected, she started wagging her tail, she started to play with the other dogs. Six months more and she was in a loving home being funny and loving. She is at times a little quirky, but they adore her and see her as a normal dog. The transformation got my attention.
Science does not know what autism is or how to treat it. Basically, researchers admit that they are trying stuff to see if it makes any difference. But as I started reading the literature, I found some intriguing connections.
Autistic children generally have high levels of serotonin in their blood platelets, but the level of “free” serotonin was low. This means that somehow the serotonin that is in the blood gets bound to the platelets but extra does not float around. This may mean high serotonin in blood cells, but low serotonin in brain.
One study suggests that this early high level could have an impact on the infant brain. Small babies do not have a formed blood-brain barrier; so high levels of serotonin could cross over and “knock out” or overload the brain. This would mean a dysfunction in the serotonin receptor system. Fewer receptor sites, or impaired receptor binding, could account for the strange combination of no impulse control and obsessive brain lock we see in autistic children. At any rate, think of impaired serotonin function in your children. It is complex and not really clear, but there is no question that serotonin in some form is implicated.
Research also comments on the fact that autistic children have high beta-endorphin levels. The literature does not reference baseline beta-endorphin but talks about an exaggerated stress response. Measuring beta-endorphin evokes stress, so the high levels they see may be a function of the exaggerated stress reaction. Stress evokes BE, and generally serotonin modulates the spike. If the serotonin system is impaired, there could be nothing to tone the beta-endorphin spike down so there would be a constant spiking and crashing.
Higher BE levels are associated with difficulty in bonding. BE is designed to kill pain, it creates “numb”. This can be life saving in a crisis, but it does not bode well for bonding. Children treated with a BE blocker actually had fewer autistic symptoms. Researchers used a drug called Naltrexone that sits in beta-endorphin receptor sites and does not allow the heightened BE reaction to charge the system. But it does nothing to heal it.
I began thinking, what about food. What do we know and how might we design a food program for your kids. The variables we are working with:
- An impaired serotonin system
- A heightened stress response
- Heightened levels of BE in response to the exaggerated stress response
OK, this simplifies the task. Here’s what we want to do:
- Have no blood sugar spiking and crashing. These evoke stress. These children need to eat every 3 hours. Three meals, on time, 2 daytime snacks and an evening snack before bed.
- No BE spiking from sugar and white things
- Increased omega 3 fatty acids to repair the brain. The brain is made of omega 3 fatty acids. If your child’s brain does not have an adequate supply, it will be brittle rather than supple. And a brittle brain overreacts even more.
What does this mean in terms of food?
Increase the protein to make sure that the brain has the amino acids it needs to make serotonin in the brain factory. This means regular and consistent protein. And yes, I know that most of your children only want to eat carbs. Think whey protein power. Identify what proteins your kids are willing to try and use those creatively.
Give your children a children’s formula of fish oil. Check the DHA formulation we have in the store. I love Nordic Naturals Products and think they are safe and very appropriate for your children.
Ultimately, you will want to move your kids to a food plan that has no wheat, no hard-core dairy (whey protein powder is ok because it does not have casein), and no sugar. Get a subscription to the magazine Living Without (www.livingwithout.com). They are great about the no wheat, no dairy part. They do not understand about the no sugar part.
Wheat and dairy contain opioid peptides and raise BE levels more. Sugar does the same. Obviously you will not do all of this at once. But you can take out things like soda and move incrementally towards the goal.
Now, at this point, you are probably either laughing or recoiling in horror. You may be thinking, “Kathleen, that is a joke, my child only eats 2 things.” I realize we have some major logistics to get through. I am very pragmatic. But, if you knew that putting your child on a protein/veggies/oil food plan with a timed evening carb would create a profound improvement, wouldn’t you want at least try? I know you have spent thousands of dollars and have tried 100 other things. We have nothing to lose. Let’s share and do problem solving together.
And, of course, it is critical that YOU do the steps. You cannot even think of making these changes with your child unless you are totally steady. Let’s do it together. I am thinking of setting a group for you to share about these issues. Let me know what you think. And here are the citations. All of the abstracts are on Pub Med if you want to read them. Go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? if you want to read them
Akbari,
H. M., H. K. Kramer, et al. (1992). "Prenatal cocaine exposure disrupts
the development of the serotonergic system." Brain
Res 572(1-2):
57-63.
Anderson,
G. M., D. X. Freedman, et al. (1987). "Whole blood
serotonin in autistic and normal subjects." J Child Psychol Psychiatry 28(6):
885-900.
Anderson,
G. M., A. W. Zimmerman, et al. (2004). "Autism clinical trials: biological
and medical issues in patient selection and treatment response." CNS Spectr 9(1):
57-64.
Blum,
I., Y. Vered, et al.
(1992). "The influence of meal composition on plasma
serotonin and norepinephrine concentrations."
Metabolism 41(2): 137-40.
Buitelaar,
J. K. (2003). "Why have drug treatments been so disappointing?" Novartis Found Symp
251: 235-44; discussion 245-9,
281-97.
Bursztejn,
C., P. Ferrari, et al. (1988). "[Metabolism of serotonin
in autism in children]." Encephale
14(6): 413-9.
Cazzullo,
A. G., M. C. Musetti, et al. (1999).
"Beta-endorphin levels in peripheral blood mononuclear cells and long-term
naltrexone treatment in autistic children." Eur Neuropsychopharmacol
9(4): 361-6.
Chugani, D. C. (2004). "Serotonin in
autism and pediatric epilepsies." Ment
Retard Dev Disabil Res Rev
10(2): 112-6.
Cook,
E. H., Jr., R. C. Arora, et al. (1993).
"Platelet serotonin studies in hyperserotonemic
relatives of children with autistic disorder." Life Sci
52(25): 2005-15.
Hollander, E., A. Phillips, et al. (2005). "A placebo controlled crossover trial
of liquid fluoxetine on repetitive behaviors in
childhood and adolescent autism." Neuropsychopharmacology
30(3): 582-9.
Humble,
M., S. Bejerot, et
al. (2001). "Reactivity of serotonin in whole blood: relationship with
drug response in obsessive-compulsive disorder." Biol
Psychiatry 49(4): 360-8.
Leboyer, M., A. Philippe, et al.
(1999). "Whole blood serotonin and plasma beta-endorphin in autistic probands and their first-degree relatives." Biol Psychiatry 45(2): 158-63.
McBride,
P. A., G. M. Anderson, et al. (1989). "Serotonergic responsivity in male
young adults with autistic disorder. Results of a pilot study." Arch
Gen Psychiatry 46(3): 213-21.
McCauley,
J. L., L. M. Olson, et al. (2004). "Linkage and
association analysis at the serotonin transporter (SLC6A4) locus in a
rigid-compulsive subset of autism." Am
J Med Genet B Neuropsychiatr Genet 127(1): 104-12.
Moore,
M. L., S. F. Eichner, et al. (2004). "Treating functional impairment of autism with selective
serotonin-reuptake inhibitors." Ann Pharmacother
38(9): 1515-9.
Mulder,
E. J., G. M. Anderson, et al. (2004). "Platelet serotonin levels in pervasive
developmental disorders and mental retardation: diagnostic group differences,
within-group distribution, and behavioral correlates." J Am Acad Child Adolesc Psychiatry
43(4): 491-9.
Nabi,
R., F. J. Serajee, et al. (2004). "Association
of tryptophan 2,3 dioxygenase gene polymorphism with autism." Am J
Med Genet 125B(1):
63-8.
Nader,
R., T. F. Oberlander, et al. (2004). "Expression of pain in children with autism." Clin J Pain 20(2): 88-97.
Nagamitsu, S., T. Matsuishi, et al. (1997). "CSF beta-endorphin levels in
patients with infantile autism." J Autism Dev Disord
27(2): 155-63.
Palermo, M. T. and P. Curatolo (2004). "Pharmacologic treatment of
autism." J Child Neurol 19(3): 155-64.
Ross,
D. L., W. M. Klykylo, et al. (1987). "Reduction of elevated CSF beta-endorphin by fenfluramine in infantile autism." Pediatr Neurol 3(2): 83-6.
Sandman, C. A. (1988). "Beta-endorphin disregulation
in autistic and self-injurious behavior: a neurodevelopmental
hypothesis." Synapse 2(3):
193-9.
Scifo,
R., M. Cioni, et al. (1996). "Opioid-immune interactions in autism: behavioural
and immunological assessment during a double-blind treatment with naltrexone." Ann Ist Super Sanita 32(3): 351-9.
Sodhi, M. S. and E.
Sanders-Bush (2004). "Serotonin and brain development." Int Rev Neurobiol 59: 111-74.
Spivak,
B., P. Golubchik, et al. (2004). "Low
platelet-poor plasma levels of serotonin in adult autistic patients." Neuropsychobiology 50(2): 157-60.
Tordjman, S., G. M. Anderson, et
al. (1997). "Plasma beta-endorphin, adrenocorticotropin
hormone, and cortisol in autism." J
Child Psychol Psychiatry 38(6): 705-15.
Tordjman, S., C. Antoine, et al.
(1999). "[Study of
the relationships between self-injurious behavior and pain reactivity in infantile
autism]." Encephale 25(2): 122-34.
Vered,
Y., P. Golubchik, et al. (2003). "The
platelet-poor plasma 5-HT response to carbohydrate rich meal administration in
adult autistic patients compared with normal controls." Hum Psychopharmacol 18(5):
395-9.
Whitaker-Azmitia, P. M. (2005). "Behavioral and cellular
consequences of increasing serotonergic activity
during brain development: a role in autism?" Int
J Dev Neurosci 23(1): 75-83.
Whitaker-Azmitia, P. M., M. Druse, et al. (1996). "Serotonin as a developmental
signal." Behav Brain Res 73(1-2):
19-29.
Whitaker-Azmitia, P. M., L. J.
Molino, et al. (1990).
"Serotonergic agents restore appropriate
decision-making in neonatal rats displaying dopamine D1 receptor-mediated vacillatory behavior." Eur
J Pharmacol 180(2-3):
305-9.
Whitaker-Azmitia, P. M., A. V. Shemer, et al. (1990). "Role of high affinity serotonin
receptors in neuronal growth." Ann N Y Acad
Sci 600:
315-30.
Willemsen-Swinkels, S. H., J. K. Buitelaar, et al. (1996). "Plasma
beta-endorphin concentrations in people with learning disability and
self-injurious and/or autistic behaviour."
Br J Psychiatry 168(1): 105-9.
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