Introduction

Our discussion earlier of Anaerobic/Dysaerobic balance was largely concerned with the functional role of lipids. We saw that lipid function was dualistic in nature. Now, as we look at prostaglandins, we will learn that lipids have a functional role not specifically associated with Anaerobic/Dysaerobic balance, and not necessarily dualistic in nature at all.

The presence of prostaglandins is ubiquitous. They appear to play some role in virtually all biochemical activity. What this means in terms of clinical practicality is that any patient with a prostaglandin imbalance will experience an increase in the symptoms associated with their underlying patterns of metabolic imbalance. For example, if a patient suffers from headaches associated with an anaerobic imbalance, the severity of the headache will be exacerbated by the presence of prostaglandin imbalance. To be maximally effective as a clinician you must be constantly aware of the potential for prostaglandins to confuse the clinical picture. With that in mind, let us look more closely at prostaglandins.

Prostaglandins are fatty acid derivatives with a multitude of physiological functions. They mediate homeostatic tissue response to stimuli and to stress of all types via:

1) the response to hormones

2) the response to neurotransmitters

3) the inflammatory response

4) platelet aggregation

5) etc.: prostaglandins appear to play some role in virtually all biochemical activity.

There are at least three series of prostaglandins, PG1, PG2, PG3. There are also lipids which function in association with PG2, e.g., prostacyclin, thromboxanes, and leukotrienes. It is intresting to note that the discovery of leukotrienes was more than 30 years after by the work of Rivici who identified these catabolic, pro-inflammatory compounds. These were Rivici’s “conjugated trienic fatty acids” associated with dysaerobic oxidative free radical tissue damage. These were the fatty acid substances which Rivici showed fixed chlorides within the cells allowing the tissues to remain excessively alkaline and therefore, exquisitely pain sensitive.

Prostaglandin Imbalance

Aberrant prostaglandin function most usually involves an excess of PG2 with respect to PG1 and PG3. Many and varied health problems can result from PG imbalances. Some of the more common include allergies, pre-menstrual syndrome, and the various forms of arthritis and other  inflammatory conditions. Associated symptoms may respond favorably to the use of PG inhibitors, e.g., aspirin,  anaprox, steroids, etc. The problem with PG inhibitors is their lack of specificity, i.e., they inhibit all PG, not just those in excess causing the condition, thereby interfering with vital physiological functions. Furthermore, while NSAIDs inhibit PG2, they have no effect on leukotrienes. Only steroids (or Oxygenic D and D-Plus) will oppose leukotrienes. Gaining symptomatic relief with PG inhibitors allows the cause of the PG imb

Excess PG2

Arachidonic acid, a common dietary fatty acid, is the precursor to PG2. Food sources of arachidonic acid include: shellfish, mollusks, butterfat, meat. Theoretically, excess intake of arachidonic acid could lead to a PG imbalance. Clinical experience has shown, however, that dietary arachidonic acid has only a minor effect on PG balance. Your patients with PG imbalance should avoid seafood, and usually butterfat, but the arachidonic acid in meat is not clinically significant.

You may recall from Chapter 5 on Anaerobic/Dysaerobic imbalance that arachidonic acid is an important factor in anti-anaerobic adrenal function. It appears that this endogenous arachidonic acid is the culprit in PG2 excess. (And is associated with the role the adrenals play in response to Anaerobic/Dysaerobic imbalances, and likely to other NUTRI-SPEC imbalances, as well.)

Excess endogenous arachidonic acid can be produced in association with several NUTRI-SPEC fundamental imbalances. It is also crucial to understand that arachidonic acid is produced from all the common dietary polyunsaturaed fatty acids (PUFA). Dietary intake of PUFA, which includes sources of linoleic acid, alpha linolenic acid, and gamma linolenic acid, will always exacerbate symptoms associated with Prostaglandin imbalance. For this reason it is most essential that your patients with PG imbalance avoid eating all the sources of PUFA – which includes fried foods, vegetable oils, salad dressings, margarine, mayonnaise and nuts and nut butters. Dietary monounsaturated fat (olive oil) does not increase the production of PG2. In fact, monounsaturates have no impact on prostaglandin synthesis of any kind. Saturated fats, on the other hand, inhibit the damaging effects of PUFA.

There is one other dietary excess which will lead to damaging levels of PG2, and that is a high carbohydrate meal. A high carbohydrate intake stimulates insulin, which activates D-5 desaturase enzyme, which increases the endogenous production of arachidonic acid. Adequate protein in the meal, however, causes a higher glucagon secretion and lower insulin secretion. The glucagon actually inhibits D-5 desaturase, thus decreasing PG2 formation. The key concept here is that the dietary ratio of carbohydrate to protein and saturated fat will control the production of prostaglandins.

Just how potentially damaging are the PG2 and associated compounds? Besides being a factor in pain, inflammation and fever, these noxious chemicals will also decrease the strength of the immune system. In particular, they will decrease the activity of natural killer cells and thus increase the risk of cancer.

PG2 is also associated with cardiovascular disease. While PG2 will increase platelet aggragation, one of its derivitives, thromboxane, is even a more powerful influence on platelet aggragation, plus causes vasoconstriction. Following endothelial damage, platelets adhere to the sub-endothelial connective tissue, releasing catacholamines, serotonin, and thromboxane. So – the thromboxane is not only associated with platelet clumping and vasoconstriction but also with proliferation of mutated endothelial muscle cells – this is the essence of the atherosclerotic lesions of cardiovascular disease. Another side note is that thromboxane is responsible for the pregnancy induced increased blood pressure you find in some women.

Another interesting point about the association between PG2 and cardiovascular disease is the relation between certain medications and PG2. It turns out that most blood pressure medications increase PG2. They do this directly by increasing catabolic/dysaerobic activity, and, indirectly by increasing insulin which, in turn, increases PG2 formation. The result is that anti-hypertensive drugs do not decrease heart attack incidence even though they do effectively lower the blood pressure. On a similar note, cholesterol lowering drugs also increase the endogenous production of arachadonic acid and thus PG2.

PG2 makes an additional contribution to cardiovascular-renal disease by virtue of its effect on the kidneys. PG2 causes vasoconstriction to the kidneys and stimulates the production of renin. PG2 also increases mineral corticoid production and thus contributes to sodium (and water) retention.

Respiratory function is also adversly affected by PG2. One type of PG2, plus leukotrienes stimulate broncho constriction. Asthma is typically associated with such an imbalance, and leukotrienes are the key here. Other respiratory allergies are associated with PG2, both directly and indirectly. The indirect effect comes from the potentiation of histamine by PG2.

No discussion of PG2 would be complete without pointing out its impact on premenstrual and menstrual symptoms. The fluid retention, breast tenderness and emotional symptoms associated with PMS (which are caused by excess estrogen) are mediated by PG2. So is the excess uterine pressure and ischemia that results in menstrual cramps.

Allergic skin reactions are also associated with PG2 and leukotrienes. Even more significant is that the conditions eczema and psoriasis are associated with excess leukotrienes. (You may recall from Chapter 5 that psoriasis is typically a dysaerobic condition.)

Finally, it has been shown that bone reabsorption at any age, and particularly osteoporosis, is associated with PG2, as is periodontal inflammation and rheumatoid arthritis.

Eicosapentaenoic acid (EPA) is a twenty carbon, five double bond, omega-3 fatty acid (20:5 n-3) which blocks endogenous arachidonic acid production. An insufficiency of EPA can contribute to excess PG2. The food source for EPA is fish oils. Endogenous EPA production can be blocked by dietary intake of trans fatty acids. Trans fatty acids are the result of processing natural fatty acids at high temperatures so that the normal cis isomer of the fatty acid is converted into the trans isomer, which is an unnatural fatty acid with no productive use in biological processes. Food sources of trans fatty acids include: hydrogenated fats such as margarine, and fats cooked under high temperature such as commercially processed vegetable oils, and fried foods. The relationship between EPA and arachidonic acid can also be upset by excess consumption of alcohol. It should also be pointed out that EPA activity requires small amounts of zinc and of vitamin B6.

Clinically managing an excess in PG2 involves maintaining a high level of EPA compared to arachidonic acid. One need not ingest fish oil as a source of EPA. More than enough EPA is produced endogenously in a person who is metabolically balanced and consuming the NUTRI-SPEC Fundamental Diet.

We experimented for many years with EPA supplementation. We have long since abandoned it as ineffective and unjustifiably expensive. To obtain any relief of prostaglandin-associated symptoms with EPA required fairly large (and expensive) doses. Furthermore, the symptomatic response faded very quickly. The key to maintaining normal EPA levels is to support endogenous
EPA production. And the way to do that is simply to maintain metabolic balance.

Insufficient PG1

A prostaglandin imbalance may involve an insufficiency of PG1 with respect to PG2. The precursor to PG1 is the fatty acid gamma linolenic acid (GLA) (18:3 n-6). The precursor to endogenous production of GLA is the fatty acid linolenic acid (18:2n-6).

The PG1 family of prostaglandins has many beneficial effects. Many of those beneficial effects counter the damaging effects of PG2. That is why we have talked in terms of maintaining an ideal ratio of PG1 to PG2.

Some examples of beneficial PG1 activity include decreased platelet aggregation, and increased renal blood flow with a simultaneous decrease in sodium retention. The renal vaso- dilating effect of PG1 is due to its inhibition of the vaso constriction effects of angiotensin and catacholamines. PG1 also stimulates renin production, which should theoretically increase blood pressure, but its effect of decreasing blood pressure via the inhibition just mentioned is stronger.

PG1 has a sedative, tranquilizing, and anti-convulsive action on the CNS. PG1 also has a calming effect by virtue of the antagonism for catacholamines that was mentioned above.

Finally, PG1 has a broncho-dilator effect. This effect is not associated with increased beta adrenergic stimulation but works by a mechanism that counteracts the effects of PG2.

As with EPA, endogenous PG1 production can be blocked by trans fatty acids, and also by excess consumption of alcohol. Other factors reducing the level of PG1 include steroids, aspirin and other anti-inflammatory drugs, lithium, and many food additives, as well as vitamin E and other anti-oxidants in high doses. Alpha linolenic acid (ALA) (flax oil) also inhibits production of PG1. Ironically flax oil is highly regarded as a nutrition supplement based on the fact that ALA is a precursor to EPA. The health food industry hype conveniently ignors the damage done by the ALA blockage of PG1 production. Adequate levels of vitamins B3, B6, C, and E, and the mineral magnesium are required to maintain normal PG1 levels.


Insufficient PG3

Prostaglandin imbalance can involve a low level of PG3 with respect to PG2. The precursor to PG3 is the fatty acid EPA which, as we have said, comes from fish oils. The precursor to endogenous EPA is ALA (18:3 n-3). Dietary ALA is, however, completely unnecessary to facilitate EPA and hence PG3 production. The NUTRI-SPEC Fundamental Diet provides everything needed for endogenous production. The only things that can prevent adequate PG3 synthesis are the various NUTRI-SPEC metabolic imbalances, and, certain pernicious practices which block PG3.

What are those pernicious practices? Once again we find that trans fatty acids and alcohol interfere with PG3 production. PG3 levels are also lowered by steroids, aspirin and other anti-inflammatory drugs, lithium, many food additives, and vitamin E or other anti-oxidants in high doses, as well as deficiencies of vitamin B3, B6, C, and E, and the mineral magnesium.

The Mega-dose Illusion

Now is the appropriate time to say a word about the presumed benefits of mega-dose nutrition therapy. The immediate but short-lived clinical benefits of megadose vitamin and mineral supplementation are frequently associated with a temporary stimulation of PG1 and PG3 synthesis relative to PG2.

Such stimulation is merely the law of mass action in effect. It is limited by the availability of the other substrates, enzymes and co-enzymes in these metabolic pathways. So, after a quick burst of activity, the metabolic pathway stalls out again, and symptoms return. Higher and higher doses of what at first appeared to be a miracle vitamin cure are taken with no beneficial effect.

A more rational alternative to megadose therapy is to supply nutritional doses of all the required nutrients, to avoid those substances which destroy PG balance, and to correct the metabolic imbalances which inhibit PG control. The clinical results obtained will be not only immediate, but permanent.


Pain and PG Imbalance

Pain often occurs with the inflammation associated with PG imbalance. This pain has a dualistic character, i.e., it is associated with the pH of the involved tissue (Anaerobic/Dysaerobic imbalance or Acid/Alkaline imbalance). However: This pain will not respond completely and permanently to a fundamental re-balancing of the tissues as long as the inflammation of the PG imbalance remains uncorrected. Therefore, it is essential to institute the PG balance regimen summarized above, as well as to treat the Anaerobic/Dysaerobic or Acid/Alkaline imbalance.

Summary of Therapeutic Regimen to Restore Prostaglandin Balance

1) Nutritional doses of Zn, Mg, Vitamins B3, B6, C, E (as found in Oxygenic B)

2) Avoid Vitamin E and other anti-oxidants in high doses (which is in perfect opposition to typical nutrition industry recommendations)

3) Strictly avoid trans fats: margarine, hydrogenated and partially hydrogenated oils, commercially processed vegetable oils, fried foods

4) Avoid PUFA: salad dressings, mayonnaise, nuts and nut butters, cooking oils, and all other vegetable oils (except olive oil and coconut oil)

5) Avoid excess arachidonic acid: shellfish; mollusks; butterfat; meat (What constitutes an “excess” varies considerably from one patient to the next.)

6) Avoid excess alcohol

7) Avoid food additives

8) Avoid steroids, aspirin and other anti-inflammatory drugs

9) Avoid lithium (in therapeutic doses)

10) There are undoubtedly many other nutrients that play a role in PG synthesis, particularly those with oxidant and anti-oxidant activity, or those commonly referred to as "free-radical scavengers" (glutathione, methionine, cysteine, beta carotene, dimethylglycine, bioflavenoids, co-enzyme Q, and bromelaine.) Specific protocol for the use of these supplements is built into your NUTRI-SPEC system. Each of these nutrients has a specific metabolic effect which dictates for which patients it is appropriate.

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