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THE NUTRI-SPEC LETTER

Volume 13 Number 9




From:
Guy R. Schenker, D.C.
September, 2002

Dear Doctor,

Your Diphasic Nutrition Plan will build around each patient a protective fortress that will last a lifetime. The benefits to your patients are felt symptomatically almost immediately, and, not only the quality but the length of life is enhanced. Your patients feel better, live longer, and get the most for their nutrition dollars. Meanwhile, you get the satisfaction and the well deserved income from offering a nutrition regimen that is not only satisfying and profitable, but easy to administer.

- You know how and to whom to administer the plan.

- You know how to personalize the plan based on a patient's age.

- You know how to personalize the plan to account for special conditions such as asthma, cardiovascular disease, diabetes, colitis, etc.

- You know how to intrude powerfully in even severe pathological conditions by recommending Diphasic A.M. and Diphasic P.M. in an initially very high quantity which descends down to the maintenance recommendation.

- You know how to do a follow-up procedure on your patients to find the ideal balance between Oxygenic A-Plus and Formula EW.

- Finally, you know that there are certain medications that must be considered "red flags" --- certain to be dragging your patient down. These medications include:

- Estrogen

- Calcium Channel Blockers

- Tylenol

- SSRIs

- (Usually) Synthroid

You already have at your disposal the information you need to pass along to your patients to convince them that estrogen and calcium channel blockers are certain to have a devastating (and even dangerous) impact on health. You also have the protocol to responsibly get your patients off these medications. If you have not received the several issue series of these Letters that explains the damaging effect of the catabolic stress hormone estrogen, along with the way to help your patients withdraw from it with minimal symptoms, then contact us immediately. Likewise, if you did not copy the last page of last month's Letter explaining, and giving the references supporting, the severe consequences of taking calcium channel blockers, let us know and we will get it to you right away.

You must have these available as handouts to distribute to your patients on these drugs. Nothing you do for these patients will have the lasting benefit you have come to expect from NUTRI-SPEC as long as they continue to take these drugs.

This month's Letter will be devoted to educating you (and your patients) on the SSRI family of antidepressant drugs.

The story on SSRI's is a fascinating example of pharmaceutical industry propaganda. Here is the story in a nutshell:

SSRI's are purported to work by increasing the level of serotonin in the brain. It is true that these drugs do increase serotonin, and it is also true that these drugs do relieve symptoms of depression in a select patient population. However, what you are about to learn, is that the sometimes beneficial symptomatic response that SSRIs produce on depressed patients has absolutely nothing to do with the fact that they raise serotonin levels.

When these drugs first came out I could not believe the story as told by the pharmaceutical companies. Through years of studying biochemistry I'd come across serotonin again and again and again as a metabolite that was active in stress reactions but that was almost entirely damaging --- contributing to platelet aggregation and all sorts of other damaging sequlae of the inflammatory process. When I heard that a class of drugs was being promoted that were beneficial because they raised the levels of this damaging chemical, I was incredulous.

As I read all the literature, the truth gradually became apparent. SSRI's raise not only serotonin levels they also potentate the activity of epinephrine, norepinepherine, and in some cases dopamine. These are neuro-active substances that are part of the catecholamine family.

As you know from your study of NUTRI-SPEC, there are certain metabolic imbalances (anaerobic, parasympathetic, and ketogenic) that are incapable of producing an adequate stress response with catecholamines. These patients are the ones that respond favorably to SSRIs but they pay a high price. Serotonin has a devastating effect on these patients --- but --- the symptomatic benefit they feel from the increase in catecholamines out- weighs the damaging effect of the increased serotonin.

In those patients that are not anaerobic, parasympathetic or ketogenic, the SSRIs generally do not produce a favorable symptomatic response, and in many cases cause terribly unpleasant side effects. In these patients, obviously, there is no benefit to increasing the catecholamine levels, and the damage from the serotonin has full impact.

On the following pages are important facts regarding serotonin and all the medications that potentiate serotonin (including 5HTP, St. John's Wort, and tryptophan supplements). The last two of these pages are references from the scientific literature from which I took the information. Please photocopy these pages and use these just like your estrogen and calcium channel blocker information to distribute to your patients.

You must get your patients off these damaging drugs.

Sincerely,

Guy Schenker, D.C.

PROZAC AND OTHER SSRI DRUGS

Regarding the Medications Prozac and the Other SSRI Drugs:
(The damaging, pro-aging effects of serotonin)

People who use Prozac and other SSRI drugs are five times as likely to commit suicide than if they took no medication at all.

Women who take these drugs are more than 7 times as likely to develop breast cancer.

These drugs can cause helplessness, apathy, aggression, and sedation.

They can worsen Parkinson’s Disease.

Serotonin elevating drugs are prescribed for stress related emotional conditions, yet the evidence is that serotonin is already too high in people suffering from emotional stress. This is because stress liberates free fatty acids from storage, which, in turn, increases the uptake of tryptophan into the brain, increasing the formation of serotonin.

Serotonin is like estrogen in its association with aggression. A record of violence has clearly been associated with above average blood serotonin levels. Note that darkness stimulates both aggression and eating.

Serotonin levels are elevated in autistic children and their relatives.

Serotonin is elevated in Huntington’s Chorea and other neurological diseases.

Serotonin is associated with some forms of panic reactions.

There is excess serotonin in the hippocampal formation of the brain in some schizophrenic patients.

Overdose with SSRI drugs can cause a sometimes fatal reaction called “serotonin syndrome.” This consists of tremors, altered consciousness, poor coordination, cardiovascular disturbances, and seizures.

The popular herbal “antidepressant” St. John’s Wort has been reported to cause “serotonin syndrome.”

Hans Selye showed that the injection of serotonin caused muscular dystrophy. Subsequent studies suggest that serotonin excess is involved in both muscular and nervous dystrophy or degeneration.

The amount of serotonin in the brain increases with old age.

Decreasing serotonin improves learning and alertness, while increased serotonin impairs learning.

Serotonin interferes with slow-wave sleep, creating a situation resembling that of depression or old age.

Serotonin causes high blood pressure and spasms of the blood vessels and promotes clotting.

Serotonin contributes to high blood pressure by stimulating both the production of cortisol and aldosterone. It also activates aldosterone secretion by the renin-angiotensin system. Angiotensin is an important promoter of inflammation and contributes to the degeneration of blood vessels with aging and stress. It also can promote estrogen production.

Serotonin stimulates cell division in connective tissues and thus contributes to the age-related thickening and fibrotic changes of soft tissues that impair organ function and thicken blood vessels.

Serotonin causes edema, histamine reactions, constriction of the bronchial tubes (asthma), suppression of the immune system, and joint swelling.

The ability to convert blood sugar into energy is impaired by serotonin. Several drugs with anti-serotonin activity are now being used to treat diabetes and its complications such as high blood pressure, obesity, and foot ulcers.

Serotonin lowers body temperature and decreases the metabolic rate.

Serotonin activates glycolysis and increases the formation of lactic acid, which interferes with cellular energy production.

Serotonin interferes with muscle mitochondria, and thus is associated with the pain sensitivity seen in Fibromyalgia.

Serotonin increases the secretion of the stress hormone, prolactin, which is known to be elevated in Fibromyalgia.

Serotonin increases the secretion of the stress hormones ACTH and cortisol (which is probably a factor influencing the rate of aging and contributes to the depression associated with aging).

Low thyroid function increases serotonin, as does excess cortisol.

Serotonin inhibits thyroid function.

Protein deficiency produces an inflammatory state that involves extreme serotonin dominance.

Stress or malnutrition either prenatally or in infancy, leads to extreme serotonin dominance in adulthood.

In animal studies, decreasing excess serotonin raises the testosterone in male animals. Drugs that inhibit serotonin synthesis tremendously increase libido.

High serotonin has been documented in preeclampsia, toxemia of pregnancy, eclampsia, and post partum depression.

Both serotonin and melatonin are potent inhibitors of progesterone release.

Serotonin is a precursor of melatonin. Melatonin lowers body temperature and decreases alertness, and suppresses thyroid and progesterone. Women who are depressed have been found to have higher daytime melatonin levels. In animal studies, supplementation with melatonin accelerates the development of tumors.

Symptoms of seasonal affective disorder including depression, pain sensitivity such as fibromyalgia, and carbohydrate craving are all increased by both serotonin and melatonin.

Estrogen (hormone replacement therapy, or birth control pills) increases the damaging actions of serotonin.

Polyunsaturated oils in the diet promote the damaging effects of serotonin. Short and medium chained saturated fatty acids have anti-serotonin activity.

Migraine headaches are often associated with excess serotonin.

Excess Serotonin is associated with the development of learned helplessness.

Role of serotonin in memory impairment. Buhot, Martin, and Segu. Ann Med 2000 Apr;32(3):210-21.

Rapid communication: Whole blood serotonin and the type A behavior pattern. Madsen, and McGuire. Psychosom Med 1984 Nov-Dec;46(6):546-8.

In vivo serotonin release and learned helplessness. Kramer, et al. Psychiatry Res 1994 Jun;52(3):285-93.

Tryptophan metabolism in children with Attention Deficit Disorder. Irwin, et al. Am J. Psychiatry 1981 Aug;138(8):1082-5.

Autistic children and their first-degree relatives: Relationships between serotonin and norepinepherine levels and intelligence. Cook, et al. Neuro-Psychiatry Clin Neurosci 1990 Summer; 2(3):268-74.

Serotonin-induced decrease in brain ATP, stimulation of brain anaerobic glycolysis. Koren-Schwartzer, et al. Gen Pharmacol 1994 Oct; 25(6):1257-1262.

Serotonin-induced swelling of rat liver mitochondria. Watanabe, et al. Endocrinologia Japonica, 1969 Feb, 16(1):133-47.

The influence of serotonin on oxidative metabolism of brain mitochondria. Mahler, and Humoller. Proceedings of the Society for Experimental Biology and Medicine, 1968 Apr, 127(4):1074-9.

Prevention of stress-induced morphological and cognitive consequences. McEwen, et al. Eur Neuropsychopharmacol 1997, Oct;7 Suppl 3:S323-S328.

Platelet secretory products may contribute to neuronal injury. Joseph, et al. Stroke 1991 Nov;22(11):1448-51.

Disseminated intravascular coagulation and acute myoglobinuric renal failure: a consequence of the serotonergic syndrome. Miller, et al. J Clin Pyschopharmacol 1991 Aug; 11(4):277-9.

Duration and distribution of experimentational muscle hyperalgsia in humans following combined infusions of serotonin and bradykinin. Babenko, et al. Brain Research 2000 Jan 24;853(2):275-81.

Neuroendocrine and substrate responses to altered brain 5-ht activity during prolonged exercise to fatigue. Bailey, et al. J Appl Physiol 1993 Jun; 74(6):3006-12.

Amino Acids and central fatigue. Blomstrand. Amino acids 2001; 20(1):25-34.

Tryptophan availability: relation to elevated brain serotonin in developmentally protein-malnourished rats. Miller, et al. Exp Neurol 1977 Oct; 57(1):142-57.

Low tryptophan diets delay reproductive aging. Segall, et al. Mech Ageing Dev 1983 Nov-Dec;23(3-4):245-52.

Sex, migraine and serotonin interrelationships. Sicuteri, et al. Monogr Neural Sci 1976;3;94-101.

A proposed pathological model in the hippocampus of subjects with schizophrenia. Scarr, et al. Clin Exp Pharmacol Physiol 2001 Jan;28(1-2):70-3.

The effect of serotonergic blockade in preeclamptic patients. Montenegro, et al. Am J Obstet Gynecol 1985 Sep 15;153(2):130-4.

Serotonin and melatonin regulate the release of insulin-like growth factor-I, oxytocin and progesterone. Schaeffer & Sirotkin. Exp Clin Endocrinol Diabetes, 1997, 105:2, 109-12.

Inhibitory role of brain stem serotoninergic neuron system on thyroid function. Ruzsas, et al. Endocrinol Exp 1979 Mar;13(1):9-18.

Diurnal and seasonal variations of melatonin and serotonin in women with seasonal affective disorder. Danilenko, et al. Arctic Med Res 1994 Jul;53(3):137-45.

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