See the web page on uric acid.
The 1905 landmark case, Jacobson v. Massachusetts, has served as the foundation for public health laws and the U.S. Supreme Court endorsement of the rights of states to pass and enforce compulsory vaccination laws. In 1922, deciding a case filed by a girl excluded from a public school (and later a private school) in San Antonio, Texas, the Supreme Court found school immunization requirements to be constitutional. Since then, courts have been generally supportive of the states’ power to enact and implement immunization requirements.
Because laws concerning immunization are state-based, there are differences in requirements across the USA. Multiple studies report an increase in the local risk of vaccine-preventable diseases when there is geographic aggregation of un-vaccinated persons.
For example, measles vaccination has been very successful in controlling a this infection. In the United States, the reported number of measles infections dropped from an average of 500,000 annually in the era before vaccination (with reported cases considered to be a fraction of the estimated total, which was more than 2 million) to a mean of 62 cases per year from 2000 through 2007.
Injuries that appear in association with vaccination have been reported and witnessed. The percentage who are injured is certainly very small but in some cases has been severe and long-lasting.
Vaccine refusal not only increases the individual risk of disease but also increases the risk for the whole community. Concerns about the consequences of vaccination must be considered against the potential for benefit not only for the person being vaccinated but the community at large.
Partially Hydrogenated Trans-fats
Your cells are defined by your membranes. They not only separate your cells from another, they also determine how your cells communicate with each other and govern their internal actions. Membranes are composed mostly of oils, with some protein and carbohydrate. The oils are continually renewed and replaced. Their composition is affected by the kinds of oils in your diet. Thus the very basic and crucial actions of cells and the proper functioning of your body are to a great extent dependent on the oils you consume every day.
The oils you consume or apply to your body are chosen in part by what is available to you from the food and cosmetics industry. It is the story of what happens when capitalism has no rules and science is supported by industry. It is odd that our government has the power and the will to force the recall of strollers and scooters, etc. when deemed unsafe yet not the will or conscience to outlaw a poison in your food – trans fats. All partially hydrogenated vegetables oils contain trans fats.
To be fair, trans fats include conjugated linoleic acid and vaccenic acid that originate in the rumenof beef, sheep, goats, and deer ending up in their meat and milk products (butter contains up to 4% trans fats). However these trans fats have different chemical configurations than the manufactured version found in processed foods.
Health and nutrition information changes so often that you may be thinking that trans fats sound like one more in a long string of things that are not good for you. Perhaps you expect that like so many other foods, trans fats will be proven to be good for us or at least not as bad as once reported. No such possibility with trans fats. There has never been any scientific evidence of benefit from trans fats.
One major reason that trans fats have been allowed to persist is that food additives in use before the FDA enacted the Food Additive Amendment in September 6, 1958 did not require FDA approval. In other words, trans fats were grandfathered in as acceptable because they were in use as of 1958.
In the late 1970’s Mary Enig, Ph.D. at the University of Baltimore showed that addition of hydrogenated vegetable oil caused disruptive life patterns and lowered disease resistance. Initially ridiculed, Dr. Enig’s research began to be proven by others. In 1982 Kritchevsky published in Federation Proceedings about the effect of trans fat on the development of atherosclerosis. Many more publications in the top medical journals such as the New England Journal of Medicine, the Lancet, Annals of Internal Medicine, etc. on the risks of trans fats appeared before our government took action. On July 10, 2002, the government’s advisor on health policy, the Institute of Medicine at the National Academy of Sciences, reported that manufactured trans fatty acids is an ingredient that has no safe level for human consumption. In the words of the report, trans fats has an “upper intake level of zero.”
Because trans fats accumulate, the poisoning is cumulative. Because there is no immediate visible effect of consuming trans fats the warning signs are missed until the damage is done years later. Here is what has been documented about trans fats thus far:
- Trans fats are absorbed in to your cell membrane where healthy essential fats should be integrated. The human lipase enzyme is ineffective with the trans configuration, so trans fat remains in the blood stream for a much longer period of time and is more prone to arterial deposition and subsequent plaque formation. Once in your cell membrane, trans fats can not be replaced.
- Trans fats irreversibly disrupt cell membrane function and communication with other cells.
- Trans fats raise LDL cholesterol and lower HDL cholesterol levels in your blood, which is the opposite of the ideal cardiovascular ratio. The Nurses Health Study I and II and the Health Professionals Follow-Up Study, Harvard School of Public Health, etc. provide consistent evidence that trans fats consumption increases the risk of coronary heart disease. Even the American Heart Association is in agreement – “Trans fats raise your bad (LDL) cholesterol levels and lower your good (HDL) cholesterol levels. Eating trans fats increases your risk of developing heart disease and stroke. It’s also associated with a higher risk of developing type 2 diabetes.” In 1994, Willett WC, Ascherio A was estimated that trans fats caused 30,000 deaths annually in the US from heart disease. (Am J Public Health 85 (3): 411–2).
- Trans fats alter arterial wall function leading to soft, weak, and stiff arteries which are susceptible to lesions, injury, and subsequent plaque formation.
- Esther Lopez-Garcia (The Journal of Nutrition 2005;135(3):562–6) studied over 700 nurses. Those consuming the most trans fat had blood levels of CRP that were 73% higher than those consuming the least trans fats. CRP is an indicator of inflammation and when elevated predicts cardiovascular disease.
- Trans fats pass from a pregnant woman’s placenta to her unborn child. The unborn child’s metabolism is adversely affected by trans fats in proportion to the amount consumed by its mother.
- Lactating mothers who consume substantial amounts of manufactured trans fats have less cream in their breast milk, since trans fats can lodge in the cellular spaces normally reserved for fatty acids. The cream is essential for maximum breast development of an infant.
- Diets high in manufactured trans fat correlate with the risk of type 2 diabetes as observed in The continuing Nurses’ Health Study I and II and the Health Professional Follow-up Study Conducted by the Harvard School of Public Health – a cohort of over 300,000 individuals.
- Trans fats inhibit the absorption of vitamin K into bones. Vitamin K is essential for healthy bone formation and strength.
- Chavarro Jorge, et al. (Proc. Amer. Assoc. Cancer Res 2006; 47) did a prospective study suggestive of a link between trans fat intake and prostate cancer.
- Research published by Anna Gosline in New Scientist (2006) indicates that trans fat may increase weight gain and abdominal fat, despite a similar caloric intake.
- M Mahfouz published a study (Acta biologica et medica germanica 1981;40(12):1699–1705) showing that trans fats are metabolized differently by the liver than other fats and interfere with delta 6 desaturase, which is an enzyme involved in converting essential fatty acids to arachidonic acid and prostaglandins both of which are important to the functioning of cells.
- In a retrospective study (Fertil Steril, 2007) involving 104 women reporting one or more pregnancies (participants in the Princeton School cardiovascular risk study) were followed for 25-30 years. Results indicate that increased dietary intake of trans fatty acids may be associated with an increased risk of fetal loss. The results also suggest that lower dietary intake of trans fat may be associated with a lower risk of fetal loss.
You would think that given the obvious and incontrovertible evidence there would not be any trans fats allowed in our food supply. Denmark became the first country to introduce laws strictly regulating the sale of many foods containing trans fats in March 2003. Other countries and cities are following suit.
However, the FDA still allows trans fats in our food supply due to the enormous influence of food and oil industries. Instead of mandating the elimination of trans fats from food as Denmark did, the FDA instituted a labeling requirement mandating that by 2006 all manufactured foods packaged foods indicate the presence of trans fats. They also gave the food processing industry a loophole. The FDA permits manufacturers to claim “zero grams trans fats” or “no trans fats” if it contains less than 0.5gm of trans fats per serving. Of course, anything can have “zero” using this method by reducing the size of the serving.
The moral responsibility of the FDA has once again been usurped by corporate rather than public interests. As a result, you must be responsible for safe guarding yourself from trans fats by reading ingredients of every label:
- Any product that lists partially hydrogenated vegetable oil, whether it is derived from soy, coconut, canola, palm, cottonseed, corn, safflower, etc. There is no oil that is safe once it has been partially hydrogenated.
- Margarine, mono hydrogenated oils, vegetable shortening, shortening, hardened vegetable oil all contains trans fats and should be avoided no matter what the label claims. Furthermore, 0.5g of trans fats is like taking a 500mg capsule of trans fats. Benecol, for example contains 0.5gm of fat per 1 ½ teaspoonfuls. You are told to use it liberally, two to three times a day. That is a large amount of trans fats! As little as 2 grams daily of trans fats was associated with a 21% increase in coronary heart disease according to the findings of the Nurse’s Study of Harvard’s School of Public Health.
- Trans fats also occur in fast foods. It is estimated that an average meal from McDonald’s contains 3 grams of trans fat. Remember the Institute of Medicine warned there is no safe level for trans fats.
- Always question advertising on any box that says: low cholesterol, no cholesterol, trans free, TFA-free, or fat-free. The FDA leaves a lot of room for hiding trans fats. Look for products that state “no hydrogenated oils” or “hydrogenated oil free.”
- This list below is not all inclusive but presents some foods that you may not equate with trans fats but were loaded with them at the time of this publication:
- Carr’s crackers. Ritz
- Some ice creams
- Belgian chocolates.
- Wheat Thins.
- Pizza dough
- Krispy Kremes donuts
- Cheese Doritos
- Packaged cheeses
- Frozen snacks (pizza, pot pies, quiches, burritos, etc)
- Cupcake and cake icings
- Pepperidge Farms Gold fish
- Microwave popcorns
- Fried foods
- Hot chocolate mixes
- Cool Whip
- Most potato chips
Foods that should not contain manufactured trans fats are all on the Page Fundamental Food Plan:
- Fresh vegetables and fruits
- Proteins from grass-fed meat, poultry, fish, eggs, etc.
- Nuts, seeds, berries
- Butter, peanut oil, extra virgin olive oil, expeller-pressed coconut oil
The term means low thyroid function. Hypothyroidism probably affects hundreds of thousands of people but is often never diagnosed. Clinical signs and symptoms of hypothyroidism include the following (1,2,3):
Low body temperature, dry skin/hair, (red hair is at particular risk for low thyroid), inappropriate weight gain and/or an inability to lose weight, brittle nails, insomnia and/or narcolepsy, poor short-term memory and concentration, fatigue, headaches and migraines, premenstrual syndrome and related problems, menstrual irregularities, depression, hair loss (including outer third of eyebrows), low motivation and ambition, cold hands and feet, fluid retention, dizziness or lightheadedness, irritability, easy bruising, skin problems/infections/acne, infertility, dry eyes/blurred vision, heat and/or cold intolerance, low blood pressure, elevated cholesterol, digestive problems (irritable bowel syndrome, acid indigestion, constipation, etc.), poor coordination, diminished sex drive, reduced or excessive sweating, frequent colds/sore throats, asthma/allergies, slow healing, itchiness, food cravings, recurrent infections, food intolerances, increased susceptibility to substance abuse, anxiety/panic attacks, yellow-orange coloration on skin (particularly palms), yellow bumps on eyelids, slow speech, thickened tongue with scallop-like indentations, fluid in the ears, etc.
Because long-term low thyroid function causes poor circulation and reduces delivery of oxygen to tissue cellular and therefore has an association with heart disease and cancer as well as making you feel miserable, having even a few of these symptoms warrants checking your thyroid function.
THE PROBLEM WITH DIAGNOSING LOW THYROID FUNCTION
With so many different symptoms and so many different organ systems potentially affected by thyroid system dysfunction, one might think that a diagnosis would be easy. However, in spite of the available blood tests for thyroid/pituitary/liver/adrenal function, the diagnosis is often missed.(1,2) One of the most common mis-conceptions regarding thyroid function is the assumption that and reliance on the requirement that the diagnosis of hypothyroidism depends on an elevated TSH level. Normally, the pituitary gland will secrete Thyroid Stimulating Hormone (hence TSH) in response to a low circulating thyroid hormone level. This is thought to reflect the pituitary’s sensing of inadequate thyroid hormone levels in the blood that would be consistent with hypothyroidism. There is no question that an elevated TSH can confirm the diagnosis of hypothyroidism, but it is far too insensitive a measure, in other words the vast majority of patients who have hypothyroidism do not have an elevated TSH level. Some have suggested that perhaps the upper limit of what is considered normal is too high, instead of the normal TSH range being from 1.0-4.5, the range of normal for TSH should be 0.5-1.5. In that way more patients would be considered hypothyroid.
Furthermore, the lab level of TSH tends to vary throughout different times during the day making it less useful to rely on as the average level. MSG (monosodium glutamate) and stress tend to lower the TSH level, for example.
The most commonly used tests of thyroid hormone levels (note that I use the term level rather than function because the two are not always equal) are the T4 (or total T4), T3-uptake, FTI (also called the T7 or Free Thyroxine Index), and total T3 (sometimes called the T3-by-RIA). These tests are also unreliable because they do not reflect the hormone level that is actually available for action. Only the free T4 and free T3 are available to act on the cells. The total T4 and total T3 (as is most commonly measured) is a mixture of protein-bound T4 and T3 (and therefore not available to the cells) and the free T4 and T3. A large percentage of patients have low levels of the free T4 and freeT3 even when all the other more commonly used tests are normal. Complicating the problem is the fact that these symptoms may present themselves while all the usual blood tests (TSH, FI, Total T3, etc) appear to be normal. When patients with Free T4 and Free T3 hormone levels below normal with or without an elevated TSH are given appropriate therapy, many report a tremendous improvement in the symptoms classically associated with hypothyroidism. Even when the labwork does not indicate low thyroid levels, many patients appear to fit the profile for low thyroid action. In fact, many of the best thyroidologists use the response to therapy as the major determinant of whether or not the patient was in fact hypothyroid. The diagnosis was confirmed by the response to the proper therapy. Even many of the most prestigious textbooks validate this approach.
Unfortunately, when the blood work does not reveal obvious low thyroid levels, many doctors are prone to refer these patients to a psychologist because they “cannot find anything wrong” with these suffering patients.(1) Obviously, the hypothyroid patient will not suffer with all of the above symptoms simultaneously. But if you have some of these symptoms, in spite of unrevealing blood tests, perhaps it is time to look further. Due to my biochemical perspective, I see features of potential low thyroid action in non-thyroid blood tests. For example, in one study 12% of women with an elevated cholesterol level were found to be hypothyroid using the TSH level. That implies that high cholesterol could represent low thyroid. A high calcium:phosphorus ratio was shown by Melvin Page, D.D.S. and others to be potentially due to low thyroid action. When the red blood cell size as measured by the MCV (see lab section on blood counts for more information) is elevated, one of the considerations is low thyroid function. Features of what Emanuel Revici, M.D. termed anabolic occur in hypothyroid conditions. He monitored salivary and urinary pH; when there is a consistently low salivary pH and a high urine pH, an anabolic state was likely. The details of this are not warranted for this discussion. The bottom line is that there may be a pattern of low thyroid activity not only in symptoms but also in the biochemical state.
The most common non-laboratory method for monitoring thyroid is basal body temperatures. Low body temperature seems to underlie many of the symptoms. Broda O. Barnes, MD, did the first studies correlating hypothyroidism to low body temperature. He found that having the patient take his/her axillary (in the pit under the arm) temperature for several mornings before getting out of bed could help document the trend correlating with the symptoms(2,3). An axillary temperature of <97.6 degrees F. indicated a hypothyroid state even when the blood tests did not show irregularities(3). Treating the patient with thyroid hormone seemed to relieve him/her of the often debilitating state(2). I would caution you on concluding that a low body temperature is only caused by hypothyroidism. See the Basal Body Temperature webpage for the proper technique and for other causes.
THYROID HORMONE REPLACEMENT THERAPY
After proper identification of hypothyroidism, the next issue is with what substance to treat. The traditional approach is to use levothyroxine (Synthroid®/Levoxyl®/Levothroid®) which is a synthetic preparation of T4. Desiccated pork thyroid (Armour®, Westhroid®, Naturethroid®) is a natural mixture of mono and di-iodothryonine and T3 and T4 that provides the entire range of thyroid hormones. Thyrolar® is mixture of synthetic T4 and synthetic T3. Cytomel® is a synthetic T3 only product that is also available. Choosing between these options is determined by finding the agent that provides the best response. Some clues to choosing the right agent are discussed below.
If the free T3 level is significantly lower than the free T4 level, it is unlikely to use treat with Synthroid/ Levoxyl/Levothroid (T4) only replacements. This is based on the assumption that if the patient could produce enough T3 from their gland or convert enough T3 from T4, then they are unlikely to do so by adding more T4. This is a key issue because T3 is 4-9 times as potent as T4. Most of the T3 found in the blood is made by the conversion of T4 into T3. The thyroid gland only makes about 20% of the T3 that is found tin the blood. Using T4-only preparations assumes that in the body it will convert to T3 in fairly standard amounts and at fairly standard rates. Unfortunately, clinical experience shows this is not true for the majority of patients. Measuring both free-T3 and free-T4 blood levels in hypothyroid patients who are on T4 only therapy proves that this is not a foregone conclusion. While a certain percentage of hypothyroid patients do convert enough T4 to T3 at a sufficient rate for T4 treatment to be adequate as a source of T3; many require both T3 and T4. In fact a recent article in the New England Journal of Medicine showed that no-one who took only T4 did better than those people who took T3 and T4 in terms of psychoemotional function, irritability, fearfulness, tension, anger, tiredness, physical coldness, nausea, etc. Thus there is certainly no advantage in using T4 alone.
You might wonder then why combination T4 and T3 products are not the first choice for all low thyroid patients. For some, pork is not well tolerated. Natural thyroid, despite what the manufacturer claims, is subject to variation between batches – not only in the exact total quantity of thyroid, but in the proportions of T3 and T4. This is rarely a problem. Another consideration is that it is probably best to take preparations that contain T3 twice a day because T3 does not stay in the blood for more than 4-6 hours. Thus, natural thyroid products are not as convenient as the once in the morning T4-only products.
In my practice, my choice is to use a combination of T4 and T3 unless I have a compelling reason not to use it. For the patient who shows no feature of persistent low thyroid function that has been on T4 only, I leave well enough alone.
Cytomel®, a T3-only product, and can be used alone or in combination with a T4-only preparations. Because T3 has a short activity (or “half life”), it needs to be used twice a day. E. Denis Wilson, MD, in his book “Wilson’s Syndrome“, found that many of patients respond best to T3-only (liothryonine). He believes there is a difference between thyroid gland dysfunction and thyroid system dysfunction. Although the TSH and T4 levels may be within the normal range, the important thing is not how much hormone is in the blood, but how effectively the T3 hormone is affecting the cells. At the present time, no tests can test the cellular function.(1) Therefore, he often diagnoses hypothyroidism by observing the patient’s symptoms. Often T3 (liothryonine) therapy will alleviate or eliminate many symptoms even those previously attributed to other causes. Dr. Wilson used T3-only because T3 is 4-9 times as active as T4.
How do I know if I’m on the right dose on thyroid. In addition to relief from many of the obvious symptoms, the basal body temperature can be a guide. As a clinical observation, I have found that when the pulse rate goes up but the temperature does not rise any more, taking more thyroid will not help. You are getting all that you will out of it and side effects or biochemical/hormonal affects from overdosage will become more and more likely.
Over-dosage symptoms, which are frequently only temporary during the adaptation stage. The symptoms may include: palpitations, nervousness, feeling hot and sweaty, rapid weight-loss, fine tremor, and clammy skin. One of the long-term results of excessive thyroid activity is osteoporosis and a tendency to stress the adrenal glands.
NUTRITIONAL AND COMPLEMENTARY THERAPIES
Less severe cases may also respond to nutritional therapy in that the glandular systems can be supported, thereby strengthening the whole body. A thorough understanding of the intricate interrelationships between body systems can provide the foundation for a sound nutritional program. A comprehensive approach will address the entire problem, not just the symptoms. Nutrition for the thyroid should include support for the adrenals, liver, pituitary and spleen. The feedback among these glands determines the levels of circulating hormones in the body(1). Because of the functional interrelationships between these organs, a deficiency in any nutrient can adversely affect thyroid function. The idea should be to promote growth, balance and repair of the thyroid and related organs.
In addition to a well-balanced whole food based multiple vitamin and mineral supplement(s), normalization of the thyroid system often responds beautifully to a multi-glandular approach without the use of thyroid hormones. Because of the body’s hormonal feedback systems, it has been proposed that taking thyroid hormones may actually induce a “welfare state” upon the thyroid gland. This means that supplying the body with its T4 hormone from without will cause the thyroid gland to cease making it on its own. I have not found this to be the case, or at least it is not universally true since many of my patients are able to adjust and in some cases discontinue taking thyroid without their hypothyroid symptoms returning. While many nutritional practitioners use thyroxine-free glandular, most of my patients prefer the more rapid and effective prescription agents.
Ray Peat, Ph.D., has written about the effect of other hormones on the thyroid system. Progesterone and pregnenolone tend to increase thyroid hormone effects because they promote the conversion of T4 to the more active T3. Estrogen has the opposite effect on thyroid hormone conversion(4). This may explain why so many women gain weight when estrogen replacement therapy or birth control pills are prescribed. Therefore, the physician needs to consider the effect of hormone replacement therapy when treating a patient for hypothyroidism.
Supplements that stress the thyroid and adrenals, such as ma huang, ephedra, guarana and excessive caffeine, should be avoided.
Anti-Thyroid effects are seen with alcohol and stress (in part from ACTH). Most pesticides are similar to thyroid hormone (both have 2 benzene rings…) and therefore can block the effect of T3. Excess cadmium or lithium.
The hypothyroid patient also needs to pay particular attention to diet. Molasses, egg yolks, parsley, apricots, dates, prunes, fish, chicken and raw milk and cheeses can supply nutrients necessary for proper thyroid function(3). On the other hand vegetables from the cabbage family should be limited and include broccoli, cauliflower, cabbage, turnips, mustard greens, kale, spinach, Brussels sprouts, kohlrabi, rutabagas, horseradish, radish and white mustard(3,5). These vegetables are often called goitrogens because they have been shown to decrease thyroid hormone production as effectively as prescription anti-thyroid drugs such as thiouracil. (5) Because these foods are antioxidant-rich, supplying other vegetables or even nutritional supplements is advisable.
- Wilson, E. Denis, MD. Wilson’s Syndrome: The Miracle of Feeling Well (2nd ed.).Orlando: Cornerstone Publishing Company, 1991.
2. Barnes, Broda, MD. Hypothyroidism: Unsuspected Illness. New York: Harper Collins Publishers, Inc., 1976.
3. Balch, James F., MD and Phyllis A. Balch, CNC. Prescription for Nutritional Healing. Garden City, NY: Avery Publishing Group, Inc., 1990, 213-214.
4. Peats Ray, Ph.D. “Thyroid: Misconceptions,” Townsend Letter for Doctors, #124, Nov., 1993, 1120-1122.
5. Goodhart, Robert S., MD, and Maurice E. Shils, MD. Modern Nutrition in Health and Disease (6th ed.). Philadelphia: Lea & Febiger, 1978, 406, 473.
MANAGEMENT RECOMMENDATIONS for CHRONIC SINUS and NASAL SYMPTOMS
Prolonged antibiotics or surgery rarely cures recurrent sinus infections. In fact there are studies indicting that a very large percentage of chronic sinus infections are not due to bacteria but yeast / fungi. Surgery does allow the sinuses a chance to drain, and if obstruction is the cause of the infections, then a “cure” may be achieved. Of course, there are many other factors that promote sinusitis. Unless these are addressed, the problem will remain and unfortunately, the bacteria or fungi may only get more resistant to the antibiotics/antifungals available. My approach is identify and correct (as possible) any of the contributing factors:
Allergies – cause the nasal lining to swell preventing sinus drainage and stimulate excess mucus production. Foods and inhaled allergens can be the culprit. By strengthening the adrenals, allergies can often be reduced to a minor nuisance. The basis for medications used to reduce inflammation (nasal steroid sprays) and decongestants are both derived from the chemicals produced by your own adrenals.
Immunodeficiency – allow even the weakest of viruses and bacteria to overgrow. Subtle immune insufficiencies may not always be associated with serious infections. Many immune disorders have a nutritional basis.
Re-infection – repetitive exposure to infectious individuals raises the risk of infection. Wash your hands! If you’ve been on antibacterials, replenish your gut flora with beneficial probiotic bacteria and you should reduce re-infections.
Gastrointestinal – as an outgrowth of the embryonic gut, the sinuses share innervation with the gut. Mucus secretion is a natural response to gastrointestinal irritation and may involve the sinuses reflexively. A healthy gut includes proper digestion, bacterial flora, mucosal integrity, etc. It is intriguing that the stomach meridian in Traditional Chinese Medicine ends over the maxillary sinuses.
Cervical/Neck – the second cervical vertebrae innervates the sinuses. Irritation of the nerve roots may promote congestion and mucus secretion that creates a favorable environment for bacterial overgrowth. A kink in the neck or subluxed disc could contribute to sinus symptoms.
Structural – an obstructed opening to the sinuses allows mucus and bacteria to accumulate. Surgically creating or improving the passageway can be curative in this case. The septum is rarely deviated enough to cause obstruction, however.
Membrane irritation – irritants that injure the mucus membrane give microbes an entryway past the primary defense barrier into vulnerable tissues. A healthy mucus membrane is key to resisting infection. Supplemental food based vitamins can visibly improve your mucus membrane barrier. Minimizing irritants will also help reduce inflammation and allow healing.
Metabolic – an over-stimulated parasympathetic nervous system may create congestion and excess mucus. Acidity is associated with a tendency to viral infections (hence the development of cold sores and canker sores with acidic foods). Other conditions promote allergies, reduce immunity, etc.
Dental – an infected dental root or implant could be supplying the sinuses with a source of bacteria.
There are three main goals in treating sinusitis in the short run:
- Decrease nasal congestion to allow the mucus to drain from the sinuses.
- Drain the infected mucus. Leaving mucus will allow the infection to hide from the antibiotic and allow the bacteria a place to re-grow.
- Eradicate the infection itself. Sinus irrigation is an option that directs the anti-microbial to the target without flooding the body just to reach the sinuses via the blood stream. As you can imagine, the sinus cavities are difficult to influence with oral medications.
For temporary relief of throat irritation, gargle with warm salt water or use Sucrets or Chloraseptic spray.
For sinus pressure discomfort, a warm moist wash cloth placed over the face and acetaminophen or ibuprofen combined with a decongestant is very effective for sinus pain.
For drainage of sinus mucus and to shrink swollen membranes, rinse the nose and sinus with SINUS RINSE. This special saline preparation has been very effective for both acute and chronic sinusitis.
The “Breathe Easy” nasal device may be helpful in maintaining an open nasal passageway, as well.
Since antibiotics also kill good bacteria in your gut, beneficial probiotic bacteria and/or an anti-yeast product is advised.
Nutritional support to fortify your immune system, strengthen your adrenals, help your mucus membranes heal, and fight the infection.
Pyroluria is a genetically determined chemical imbalance involving an abnormality in hemoglobin synthesis. Hemoglobin is the protein that holds iron in the red blood cell. Individuals with this disorder produce too much of a byproduct of hemoglobin synthesis called “kryptopyrrole” (KP) or “hemepyrrole.” Kryptopyrrole has no known function in the body and is excreted in urine.
Kryptopyrrole binds to pyridoxine (vitamin B6) and zinc and makes them unavailable for their important roles as co-factors in enzymes and metabolism. These essential nutrients when bound to kryptopyrrole are removed from the bloodstream and excreted into the urine as pyrroles. Arachidonic acid (an omega-6 fatty acid) also becomes deficient.
The effect of pyroluria can have a mild, moderate, or severe depending on the severity of the imbalance. Most individuals show symptoms of zinc and/or B6 deficiencies, which include poor stress control, nervousness, anxiety, mood swings, severe inner tension, episodic anger (an explosive temper), poor short-term memory and depression. Most pyrolurics exhibit at least two of these problems. These individuals cannot efficiently create serotonin (a neurotransmitter that reduces anxiety and depression) since vitamin B6 is an important factor in the last step of its synthesis. Many of these persons appear to benefit from SSRI medications such as Prozac, Paxil, Zoloft, Celexa, etc. However, as with all mind-altering drugs, side effects occur and the true cause of the mental difficulties remains uncorrected. In addition these individuals often have frequent infections and are often identified by their inability to tan, poor dream recall, abnormal fat distribution, and sensitivity to light and sound. As you can imagine an SSRI will not correct these metabolic effects. More healthful benefits may be achieved by giving the appropriate supporting nutrients.
Pyroluria is detected by chemical analysis of the abnormal
pyroles in urine detectable as a purple (on testing paper) metabolite in called “the mauve factor.” Most persons have less than 10mcg of KP per deciliter. Persons with 10-20 mcg/dl are considered “borderline” pyroluric and may benefit from treatment. Persons with levels above 20 mcg/dl are considered to have pyroluria, especially if the above symptoms are present>.The chemical analysis for KP is difficult due to the tendency for this chemical to decompose. Sometimes it is necessary to repeat the urine test to properly determine the level of KP being excreted. To make the initial diagnosis, no vitamins or minerals should be taken for two days before the urine is collected (This is to avoid false negative results). The specimen should be handled properly as well – collected and frozen immediately and protected from any light by being placed in aluminum foil. A repeat test to determine if the condition has been improved may be helpful.
People with mild-moderate pyroluria usually have a fairly rapid response to treatment if no other chemical imbalances are present. People with severe pyroluria usually require several weeks before progress is seen and improvement may be gradual over 3 – 12 months. Features of pyroluria usually recur within 2 – 4 weeks if the nutritional program is stopped. Thus, the need for treatment is indefinite.
Pyroluria is managed in part by restoring vitamin B6 and zinc. The type of replacement therapy is very important as zinc must be provided in an efficiently absorbed form. Vitamin B6 is also available in several forms. Both zinc and B6 supplementation need to be directed by the doctor as too much can be toxic, use of the wrong form will be ineffective, and avoiding competing minerals and supplements may be necessary. Other nutrients may assist in pyroluria include niacinamide, pantothenic acid, manganese, vitamins C and E, omega-6 fatty acids and cysteine. Food sources and nutritional supplements containing copper and red/yellow food dyes should be avoided.
Because pyrolurics are stress intolerant, they seem to be especially vulnerable to cumulative stress over many days. For example, parents of a pyroluric child should use discipline that is “short and sweet” rather than “long and lingering.” It is not unexpected that pyroluric patients are prone to relapses, especially during illness, injury, or emotional stress.
Much of the information we have about pyroluria is from the work of the late Carl Pfeiffer, M.D. in the 1970’s. Some references include:
Irving DG: Apparent non-indolic ehrlich-positive substances related to Mental illness. JNeuropsychiat, 1961;2:292-305.
Hoffer A, Mahon M: The presence of unidentified substances in the urine of psychiatric patients. JNeuropsychiat, 1961;2:331-397.
Irvine DG, Bayne W, et al: Identification of kryptopyrrole in human urine and its relationship to psychosis. Nature, 1969;224:811-813.
Pfeiffer CC, Lliev V: Pyrroluria, urinary mauve factor, causes double deficiency of B6 and zinc in schizophrenics. Fed Proc, 1973;32:276.
Jackson JA, Riordan HD, Neathery S: Vitamins, blood lead and urine pyrroles in Down Syndrome patients.Amer Clin Lab, 1990:Jan- Feb:8-9.
Jackson JA, Riordan HD, Neathery S, Riordan N: Urinary pyrroles in health and disease. J Orthomol Med, 1997: 12;2:96-98.
Hormones and the Menstrual Cycle
The ovary and the adrenals are the source of two types of “female” hormones, estrogens and progesterone. At least six different estrogens have been identified, but only estrone, estradiol (E2), and estriol are circulate in significant quantities in the blood. Estrogen levels begin to increase during the first part of the menstrual cycle, (follicular phase) peak just before ovulation, and then decline slowly until they reach their lowest point at the onset of menses. The principal function of the estrogens is to cause cellular proliferation and growth of the tissues of the sexual organs and tissues related to reproduction.
Progesterone is a hormone that prepares the lining of the uterus for the fertilized egg and maintains pregnancy. The name tells the story, promotes gestation hormone. Progesterone is derived primarily from the corpus luteum in the ovary after ovulation. When the follicle ruptures, it is transformed into the corpus luteum. Progesterone is also produced by the placenta during pregnancy and in small amounts by the adrenal cortex. Progesterone is a “precursor” hormone that is converted into other steroid hormones like testosterone, estrogens, cortisol and aldosterone.
During the follicular phase (before ovulation), the concentration of progesterone in the bloodstream is less than 1 ng/ml, although still present in much higher amounts than estrogen. Ovulation initiates the second half (luteal phase) of the cycle, and at this time progesterone levels in the blood increase up to 20 ng/ml and may be 140 times as high as estrogen. As its levels increase, progesterone acts as a powerful antagonist to the action of estrogens. A sharp decline in progesterone initiates the onset of the menses.
Pre-menstrual syndrome (PMS) affects millions of women to varying degrees. It has been estimated that 7090% of all women regularly experience at least one symptom of PMS and in 10-20% of women symptoms are severe enough to be incapacitating. Once dismissed as female neurosis or physical frailty, PMS is now a recognized medical entity that clinically characterized as the cyclical occurrence or exacerbation of one or more physical or psychological symptoms during the luteal phase (after ovulation) of the menses. Symptoms, which include irritability, emotional lability, bloating, breast tenderness, hypoglycemic symptoms, food cravings, weight gain and depression, improve or generally disappear entirely with the onset of the menses.
While numerous hypotheses have been advanced to explain the etiology of the syndrome, most have centered on the ovarian hormones, estrogen and progesterone and the balance between them. No one explanation suffices to explain all types of PMS, but it is generally held that many cases are caused by elevated levels of estrogen, resulting from excessive endogenous production or from a failure of the liver to adequately metabolize estrogens to their excretable forms. A concomitant theory (since progesterone is biologically an antagonist to estrogen) posits low progesterone, or progesterone lowin relation to estrogen as the cause of PMS. An excess of prolactin, elevated free luteinizing hormone levels, and deficiency of brain amines (serotonin and dopamine) are also considered to be involved either independently 3 or as a consequence of the estrogen-progesterone ratio.
Initial efforts to manage PMS by administering progesterone were complicated by unsatisfactory ways of delivering the hormone. Because of the importance of protecting the human organism from the effects of hormones from other species that may be consumed in the diet, a sophisticated system exists to eliminate them. Hormones that are taken orally are shunted first to the liver, where they are converted to less active forms for elimination. This first-pass by the liver makes supplementing with oral hormones difficult. In fact in a leading medical text, Harper’s Biochemistry, “progesterone is ineffective when given orally.” Twenty-five years ago a British physician, Katherina Dalton, M.D., began using progesterone to treat PMS. She obtained good clinical results using intramuscular injections, vaginal suppositories or rectal pessaries of natural progesterone. Her pioneering work prompted others to use natural progesterone in non-oral forms, which has been used successfully now by doctors all over the world for decades.
Exercise and avoiding caffeine, refined carbohydrates, and alcohol also help reduce PMS. In addition, certain types of PMS respond to magnesium, vitamin E, essential fatty acids, and/or vitamin B6. These nutrients modulate hormones and chemicals in the brain that appear to be the primary contributors to PMS. For example, vitamin B6 is a coenzyme in the final step of the formation of dopamine and serotonin. These two biochemicals play a role in mood, anxiety, depression, stamina, sleep, etc. Excessive levels of estrogens, which compete with B6, may lead to a diminished biosynthesis of serotonin from tryptophan.
Natural vs Synthetic Progesterone
It is important to distinguish between the “natural” progesterone successfully used by Dr. Dalton and synthetic progestational agents such as progestins, progestagens or gestoizens that are present in oral contraceptives. Progesterone refers to a specific molecule, the hormone produced by the ovaries or adrenal glands. All progestins are synthetic hormones that closely resemble progesterone, but differ in important ways. The natural and synthetic hormones share the ability to sustain human secretary endometrium but progestins do not have the full range of biological activity of progesterone.Progestins are associated with a wide range of undesirable side effects that often undermine patient compliance. Significantly, progestins’ appear to inhibit biosynthesis of progesterone, lowering serum levels of the hormone and aggravating conditions linked to inadequate progesterone.5 Synthetic progestins lower the “good” HDL cholesterol and reverse the benefit of estrogen on heart disease.
In Lorraine A. Fitzpatrick, M.D.’s August 1999 Mayo Clinic study of 176 women taking natural oral progesterone after they had taken synthetic progestins, 34% felt more satisfied with the natural progesterone compared to the prior progestins. The women reported 50% improvement in hot flashes, 42% improvement in depression, and 47% improvement in anxiety. The natural oral “progesterone also controlled breakthrough bleeding better than the synthetic hormone.”
Several species of the yam family (dioscoreaceae, also called barbasco in Central America) as well as soybeans, contain significant amounts of diosgenin, a complex molecule which converts readily and inexpensively to pregnenolone and then into a “natural” progesterone which is essentially identical to the hormone produced in a woman’s body. Both progestins and the “natural” progesterone derive from diosgenin, but because a natural hormone cannot be patented by a pharmaceutical company, an alteration of the molecule was required in order to secure patent rights … hence progestins.
Female athletes who exercise to the point of having anovulatory cycles with subsequent loss of progesterone experienced bone loss despite normal levels of estrogen levels.9
Given the first-pass liver loss with oral progesterone preparations and the inconvenience of injections and suppositories, a different route of administration of the natural progesterone is highly desirable. The development of transdermal creams containing progesterone combined with plant extracts containing diosgenin have proved to be a very effective alternative. Since transdermal absorption bypasses the liver, smaller amounts of progesterone are required to accomplish results. Over the past 10 years enough clinical evidence has accumulated to verify that topical natural progesterone is an effective tool for the management of a majority of PMS cases.6
Progesterone and Menopause
By the time a woman reaches menopause, gonadal hormone production, which has been on a slow, steady decline since her 30’s, reaches its lowest point. With the exception of small amounts produced by the adrenal cortex, a woman’s production of both progesterone and estrogen after the menopause is negligible, and the biological consequence of this loss are dramatic.
For decades the focus of research on the climacteric and its health risks was exclusively on estrogen (specifically, synthesized estradiol) probably because it was regarded as the most potent of the female hormones. Additionally, it was known to mediate the activity of osteoclasts (bone resorption cells), an important consideration in light of the risk of serious health consequences of osteoporosis. Despite a growing list of concerns surrounding the use of supplemental estrogen (including increased risk to cancers of the breast, cervix, and endometrium) it has for years been the standard of care for menopausal complaints and the prevention of osteoporosis.
Progesterone and Osteoporosis
While conventional estrogen replacement therapy (ERT) does retard bone resorption and decreases the incidence of fracture for a number of years it does not stop or reverse the progressive dismantling of bone.7 As concerns regarding the side effects of ERT continued to mount estrogen began to be paired with progestins to balance the tissue stimulating effects of estrogen and confer protection against estrogen-related cancers. Analysis of several studies on the effect of combined progestin-estrogen therapy indicates that progestins do appear to improve bone density, but their use is accompanied by a long list of unacceptable potential side effects.
Since these observations, the role of natural progesterone in osteoporosis has been investigated, most notably John Lee, M.D., a California clinician and researcher. In a recent article, Dr. Lee reviewed several important observations concerning the role of progesterone in bone formation:’
The correlation of osteoporosis with hormone decline is stronger for progesterone than for estrogen. Bone loss begins well before the actual onset of menopause, a time when estrogen is still sufficient but when progesterone levels have already begun to decline.
There is evidence of progesterone receptors in osteoblasts (bone building cells) but not for estrogen, indicating a bone-building role for progesterone.10
In the early 80’s Dr. Lee began using transdermal progesterone (derived from wild yams) to treat his female osteoporotic patients. Initially, it was prescribed in conjunction with estrogen, but later used alone (except in cases of vaginal dryness), with a program of vitamins, modest calcium supplementation, and dietary advise. Bone mineral density (BMD) was monitored by lumbar dual photo absorptiometry, and other factors such as hypothyroidism and achlorhydria were adjusted as required. Dr. Lee observed BMD increases of 10-15% within 6 months and 20-25% in 3 years.Mean 3-year increase in BMD was approximately 15% with even greater increases in those with the lowest initial BMD. Therapy produced relief of bone pain, increased physical activity, height stabilization, and fracture prevention. The benefits of progesterone were independent of age, time from menopause, or estrogen use.”
Other significant benefits were observed in Dr. Lee’s patients: Women with endometrial hyperplasia when using estrogen alone reverted to normal endometrium on progesterone. Women who experienced fibrocystic breast disease while on estrogen alone reported improvement. Similarly, women who developed hypertension while on estrogen became normotensive when switched to progesterone. Lipid profiles improved, and a general feeling of well being without unpleasant side effects was characteristic of his patients.
Other menopausal symptoms, including hot flashes, night sweats, declining libido, and emotional irritability/ lability also respond well to progesterone therapy. Some patients reported an improvement in skin quality, and a decrease in “brown” spots.
2. Gaby, Alan. The Doctor’s Guide to Vitamin B6, Rodale, 1984, p. 25.
3. London, R. et al. Evaluation and Treatment of Breast Symptoms in Patients with PMS. Journal of Reproductive Medicine, 1983;28: 503-508.
4. Chakmakjian, Z. A Critical Assessment of Therapy for the Pre-menstrual Tension Syndrome. J. of Reproductive Medicine 1983;28: 532-537.
5. Whittaker, N. PMS and Post-partum Depression, Mothering 1983: 27-34.
6. Kamen, Betty. Hormone Replacement Therapy, Yes or No, Nutrition Encounter, Inc. 1993: 210.
7. Lee, John. Successful Menopausal Osteoporosis Treatment Restoring Osteoclast/Osteoblast Equilibrium. Townsend Letter for Doctors, 1994; 133-134
8. Ibid. 900-905.
9. Prior, J, Vigna Y. Spinal bone loss and ovulatory disturbances New England JMedicine 1990; 323:1221-7
10. Prior, J. Progesterone as a bone-trophic hormone, Endocrine Reviews 1990; 11: 386-398.
11. Lee, John. Osteoporosis Reversal, The Role of Progesterone, International Clinical Nutrition Review, 1990; 10:384-391.
There are several types of premenstrual symptoms, each has a specific underlying cause. No one treatment will correct all types. As you read through the profiles described, one will match most of your symptoms. Focus on that profile for a better understanding. At the bottom of the weboage are more information about the particular effects of estrogen and progesterone.
PREMENSTRUAL SYNDROME SUB-TYPE A: Nervous tension, mood swings, irritability, anxiety, and insomnia
- Estrogen stress (with secondary brain dopamine depletion due to estrogen’s stimulation of MAO-2 activity causing lack of “relaxing” neurotransmitters and inhibition of MAO-1 activity causing excess norepinephrine/epinephrine excitatory brain transmitters. As a drug, MAO-inhibitors are used to treat depression…)
- Low progesterone production causes anterior pituitary stimulation leading to increased ovarian estrogen production
- Ovarian cysts or tumors
- Adipose tissue aromatization of androgens into estrogen
- Insufficient liver clearance of estrogens (see #8)
- Inadequate biliary flow
- Low fiber reducing intestinal clearance of conjugated estrogens
- High fat diets promote hydrolysis of intestinal conjugated estrogens into free estrogens that are reabsorbed.
- Enzymatic conjugation of estrogen in the liver is magnesium-dependent, if magnesium deficient there may be difficulty in metabolizing estrogen properly.
- Low B6 impairs estrogen utilization and removal by deactivation of the hormone itself. It may also be due to vitamin B6 antagonism by yellow dyes and hydrazine
- Excessive vitamin E elevates estrogen levels
- Progesterone insufficiency (a CNS depressant by inhibiting MAO-2 leading to increased brain dopamine and stimulates MAO-1 leading to decreased excitatory neurotransmitters)
- Elevated estrogen inactivates the corpus luteum, where progesterone is produced
- Low LDL cholesterol bioavailable for progesterone production
- Excessive vitamin E (>600IU) lowers LDL cholesterol (lower doses stimulate progesterone production)
- Excessive animal fats/arachidonic acid lead to excessive PGF, which directly inhibits progesterone synthesis
- Insufficient vitamin E inhibition of arachidonic acid release (and thus PGF formation)
- Insufficient vitamin E effect as luteotrophin
- Excessive hepatic clearance of progesterone by synthetic progestin use or barbiturates
- Adrenal fatigue with insufficient progesterone production
- Hyperadrenia with resultant suppression of ovarian function via anterior pituitary response to the rapid oxidation
- Dopamine depletion
- Chronic physical or psychological stress
- Depletion from magnesium deficiency
- Insufficient vitamin B6-dependent conversion of tyrosine to dopamine
- Vitamin B6 deficiency blocks dopamine synthesis at renal levels
- Excess excitatory neurotransmitters
- Estrogen > Progesterone effect
- Refined sugar favors conversion of tryptophan to serotonin causing a relative dopamine deficiency and acetylcholine deficiency, which causes disturbances in movement and memory
Diet considerations for subtype A PMS: Tend to have excessive dairy product (Ca++>Mg++), high fat and/or refined sugar intake.
PREMENSTRUAL SYNDROME SUB-TYPE C: (relative hypoglycemia with craving for sweets, increased appetite, heart pounding, dizziness or fainting, fatigue, headache, etc.)
- Estrogen excess with symptoms primarily due to relative hypoglycemia. Often with low magnesium and prostaglandin E1 with increased carbohydrate tolerance
Management considerations for sub-type C PMS: Avoid alcohol since it impairs the release of glucose from liver glycogen. Eat small meals regularly.
PREMENSTRUAL SYNDROME SUB-TYPE D: Is uncommon. (Depression, forgetfulness, crying, and confusion). May see high progesterone levels and, in some with excess hair growth, adrenal androgens. Others have lead intoxication.
- Estrogen deficiency
- Ovarian fatigue from adrenal suppression
- Ovarian failure, ablation, or surgery
- Estrogen antagonism
- Reduced estrogen binding by lead
- Relative Progesterone excess
- Deficiency of norepinephrine in the central nervous system
- Decreased synthesis from insufficient dietary tyrosine
- Chronic stress-induced tyrosine depletion
- Increased metabolism of norepinephrine due to increased MAO-1 activity (Estrogen > Progesterone)
PREMENSTRUAL SYNDROME SUB-TYPE H: (Weight gain, swelling of extremities, breast tenderness, and abdominal bloating)
- Excess estrogen
- Intake of too much refined sugar leads to sodium and water retention by hypoglycemic and acidotic stimulation of adrenals
- Excess aldosterone with resultant water and salt retention
- Chronic stress leads to ACTH release from Anterior Pituitary
- Elevated serotonin causes ACTH secretion
- Acidosis stimulates the adrenals
- Elevated estrogen leads to angiotensin II release, which in turns leads to ACTH secretion
Management considerations for this subtype H PMS: Caffeine and other methylxanthines and nicotine exacerbate so eliminate these. Eliminate refined carbohydrates.
CRAMPS: If there is pain and cramping during but not before menses, this pattern suggests an imbalance of prostaglandins, calcium loss in anaerobic metabolism or thyroid stress, estrogen insufficiency, progesterone excess, or sympathetic nervous system stress.
EXCESSIVE BLEEDING: If the menstrual flow lasts only 2-3 days, the pattern suggests relative estrogen excess. If the menstrual flow last for more than 3 days, the pattern suggests progesterone insufficiency. Other factors that lead to excess menstrual flow are low blood clotting factors due to deficiency of vitamin K, lack of ionized calcium, parathyroid insufficiency, liver insufficiency, fibroids, and malignancy.
PAINFUL OVULATION: May be due to pelvic congestion due to progesterone insufficiency or estrogen stress
Estrogen is produced by the ovarian follicle under the influence of FSH, which is produced in the anterior pituitary. Production is stimulated by vitamin E, which also reduces breast symptoms. Vitamin B6 reduces blood estrogen and aldosterone, and may increase intra-cellular magnesium levels. Estrogen is mildly anabolic with an anti-dysaerobic effect. These metabolic states are discussed in more detail under aerobic metabolism. High fiber vegetarian diet binds estrogen in the gut and prevents its reabsorption during enterohepatic re-circulation. Estrogen decreases the cycle length and causes fat deposition in the breasts.
Estrogen Insufficiency: Causative factors include ovarian or pituitary insufficiency, intestinal bacteria destroyed so there is no de-conjugation in the intestine and re-circulation back into the body. The effects of low estrogen may include:
- Increased diastolic blood pressure
- Pain, cramping, & tension DURING but not before menstruation
- Decreased menstrual blood flow
- Menstrual cycle longer than 28 days
- Hypoplastic weak uterus and senile vaginitis
- Menopausal hot flashes
- Poor retention of sodium, chloride, potassium and calcium.
- Poor calcium assimilation
- Excess retention of phosphorus
Estrogen excess: Can be due to adrenal insufficiency with ovarian overcompensation, liver overload preventing estrogen breakdown, parasympathetic dominance, excess fat or fiber intakes effect on enterohepatic circulation, excess coffee, tea, chocolate, or vitamin E. Features of a relative estrogen excess may include:
- Reduced diastolic blood pressure
- Pre-menstrual tension, nervousness, headaches, nausea, & fluid retention
- Menstrual cramps due to increased extracellular K+ and decreased Ca++ = smooth muscle spasm
- Watery vaginal discharge
- Excess menstrual flow lasting only 2-3 days
- Decreased thyroid effect with reduced temperature
- Tendency to vein problems
- Tendency to schizophrenia
- Increased incidence of breast, lung, liver, and GI cancer
- Gynic qualities
- Increased calcium & phosphorus retention
- Poor absorption of phosphorus
Progesterone is produced by the corpus luteum under the influence of LH. Low progesterone may be the result of thyroid insufficiency (which may be secondary to adrenal, anterior pituitary, or estrogen stress). Progesterone is mildly catabolic, is anti-dysaerobic, and opposes estrogen. Placental and mammary concentrates have progesterone activity. Progesterone decreases bleeding.
Progesterone Insufficiency: May be due to thyroid insufficiency. Also see webpage devoted toprogesterone…
- Menstrual cycle shorter than 28 days
- Heavy menstrual bleeding
- Fluid retention during menses
- Premenstrual tension, nervousness, headache, nausea, and fluid retention
- Menstrual bleeding longer than 3 days
- Menstrual cramps
- Uterine fibroids
- Breast lumps
- Breast swelling with increased subcutaneous fluid
- Decreased systolic blood pressure and pulse pressure
- Pulse and temperature decreased
- Poor retention of sodium and chloride
- Vomiting and toxemia of pregnancy
- Uterine contractions during early pregnancy
- Habitual miscarriage
Progesterone Stress: May be due to incomplete breakdown by liver, anaerobic, sympathetic, or glucogenic imbalances. Features of relative progesterone excess may include:
- Menstrual cycle longer than 28 days
- Scanty menstrual flow
- Acne during menses and/or acne, greasy hair and skin
- Breast tenderness during menses
- Premenstrual depression
- Increased temperature
- Dry vagina and/or thick discharge
- Excess retention of sodium, chloride, phosphorus and sulfur
The metabolism of carbohydrates, proteins and fats into energy is referred to as oxidation. Energy is formed and released at different stages during two cycles – glycolysis and the Citric acid cycle. To get the most energy out of foods, both cycles need to work at the right rate. If carbohydrates and amino acids are oxidized too slowly (“slow oxidation”) in one cycle or too quickly in another cycle (“fast oxidation”), energy production is reduced. Both fast and slow oxidizers suffer from inefficient energy production, but for opposite biochemical reasons. The most common symptoms of a fast or slow oxidative rate are FATIGUE, EMOTIONAL DURESS of some type, LOWERED RESISTANCE to infections, a LOW BODY TEMPERATURE, GALL BLADDER or LIVER PROBLEMS, and being over or under WEIGHT. Your oxidation rate is influenced by both genetics and by your diet. Thus, what you eat affects your rate of oxidation and energy production which in turn affects your mental, emotional, behavioral, and in some cases, physical characteristics.
THE SLOW (KETOGENIC) OXIDIZER
Generally speaking, the characteristics of slow oxidation tend to be of the alkaline, hypo-active quality. Slow oxidizers tend to have very little appetite, an aversion to heavy proteins and fats, low but steady energy levels, depression, digestive problems due to lack of hydrochloric acid production, calcium deposits, poor fat metabolism, apathy, lethargy, repressed emotions, introversion, belching, pre-mature aging, and often feel cold. A slow oxidizer often finds he/she thinks and feels better if after a heavy dinner he/she does not eat anything after arising the next morning. For this reason he/she should not eat a heavy breakfast. High intensity, short duration exercise is poorly tolerated and for the slow oxidizer needs to be of low intensity and long duration (aerobic).
Slow oxidizers have problems metabolizing carbohydrates and tend to have higher blood sugar levels (hyperglycemia) after an oral glucose tolerance test. Slower oxidizers have lower levels of blood lipid (cholesterol, triglyceride) and citric acid cycle intermediates and higher levels of pyruvate and lactate. They tend to be able to hold their breath for a relatively long period and have a relatively lower pulse rate.
Dietary recommendations for the Slow oxidizer:
PROTEINS: low fat, low purine variety such as selected fish, chicken, turkey, eggs, low fat dairy
SUPPLEMENTS: Emphasize activated vitamin B1, B2, and B6, niacin., and potassium citrate, magnesium citrate and chloride, copper, manganese aspartate, and iron. PABA, vitamin C and D, and chromium are also recommended.
Eat a light breakfast (that contains protein) and restrict calcium.
ALLOWED IN MODERATION
Whole fruits, lean beef, lamb, natural and whole grains, breads and cereals, cold-processed non-hydrogenated vegetable oil (ex: olive is preferable source).
HIGH FAT or HIGH PURINE PROTEINS: fatty red meat, salmon, tuna, herring, anchovies, high purine proteins such as liver, caviar, meat concentrates, artichoke hearts, and modest purinecontaining foods such as beans, peas, lentils, cauliflower, spinach, and asparagus.
FATTY FOODS: lard, butter, oils, fatty meats, nuts, avocado, high fat pastries low in flour such as cheese cake, Danish, torts, peanuts, and peanut butter . High fat content DAIRY products like cheese and cream.
CARBOHYDRATES: sugars, fruit juices, alcoholic beverages, and meals consisting mainly of starches and sugars.
See the bottom of webpage for other notes about the slow oxidizer diet…
THE FAST (GLUCOGENIC) OXIDIZER
Generally speaking, the characteristics of fast oxidation tend to be of the acid, hyper-active quality. Most women tend to be fast oxidizers. Fast oxidizers tend to have strong appetites, crave and do well on heavy proteins and fatty foods, tend to get hyper yet feel exhausted underneath, feel anxious, nervous, jittery, have severe emotional ups and downs, feel too warm, irritable, impatient, are competitive and usually extroverted.
Fast oxidizers tend to have low blood sugar (reactive hypoglycemia) and higher levels of blood cholesterol and triglyceride and citric acid cycle intermediates. Bilirubin is commonly found in the urine. They tend to be unable to hold their breath a long period (one can consider the fast oxidizer functionally anemic due to low oxygen capacity in the blood) and have a relatively faster pulse rate. Exercise should be of high intensity and short duration (anaerobic) if normal or underweight but aerobic (walking, biking, etc.) if overweight.
FOODS RECOMMENDED for a Fast Oxidizer
FATS/PROTEINS: all meats (especially beef, lamb, and venison), fish (especially tuna and salmon) and fowl, especially high fat, high purine (adenine) types: such as anchovies, brains, meat gravies, soups, heart, herring, caviar, kidney, liver, sweetbreads, mussels, sardines, tuna, and meat extracts. Foods with moderate purine content include meat, shellfish (clams, crabs, lobster, oysters, shrimp), asparagus, cauliflower, spinach, lentils, yeast, whole grain breads and cereals, beans, peas, mushrooms, and peanuts.
NUTS & SEEDS: almonds, walnuts, peanuts, peanut butter, sunflower seeds
CARBOHYDRATES: cauliflower, beans, peas, lentils, broccoli, barley, corn, sprouted grains (sprouting destroys the phytates that bind calcium*)
SUPPLEMENTS: Your supplement should contain vitamin A, vitamin C, vitamin E, vitamin B12,niacinamide, calcium pantothenate, bioflavonoids, choline, inositol, calcium, phosphorus, iodine, and zinc. Carnitine.
Eat a full breakfast. Eat frequently
ALLOWED IN MODERATION
PROTEINS: milk, buttermilk, cottage cheese, eggs
VEGETABLES: root vegetables (carrots, beets, yams, potatoes, radishes, onions), lettuce, green peppers, cabbages, pickles, cucumbers, and tomatoes
SWEETS & STARCHES:- simple carbohydrates like glucose, maltose, fruit juices, honey, corn syrup, highly glycemic foods like white bread, white rice, soft drinks, catsup, and meals consisting mainly of starches and sugars.
MISCELLANEOUS: spices, sauces, alcohol, and caffeinated drinks such as coffee, colas or tea.
SUPPLEMENTS: limit vitamin B1 (thiamine) and vitamin B3 (niacin) because they increase Coenzyme A and accelerate carbohydrate oxidation; vitamin B2 (riboflavin) and vitamin B6(pyridoxine) because they increase the breakdown of amino acids leading to a faster citric acid cycle activity and more CO2 generation; glucogenic amino acids (Alanine, Glycine, and Serine), and citrates.
NOTES ABOUT either a SLOW or FAST OXIDATIVE RATE
- Never eat a meal that is predominantly carbohydrates. Avoid all “trans” fats (hydrogenated vegetable oils).
- Any sharp shift in the weather tends to further disturb one’s metabolism in the direction it normally tends. Fast oxidizers go faster, and slow oxidizers go slower.
- Common pesticides, paints, and chemicals can disturb the energy producing abilities of tissues.
- In addition to knowing what foods to use sparingly and what foods to emphasize – make sure the core of your diet contains enough of the correct type of protein at every meal (about 1 gram per kilogram/2.2 pounds of ideal body weight a day*). The metabolites of protein-derived sugar is stored in the liver as glycogen and is converted to glucose when sugar derived directly from carbohydrates in the diet runs out. The gradual digestion of protein keeps an adequate and continuous glycogen (and thus blood sugar) reserve. That is not to say protein can be substituted for sugar and starch in the diet, for without available glucose, protein can not be converted into glycogen.
- Alcohol depletes glycogen storage in the liver causing an increase in blood sugar. Alcohol also increases the demand for carbohydrates (by being directly broken down into acetyl CoAof the Tricarboxylic Acid Cycle) and the resultant nutrients needed to metabolize it. If you think you “need a drink,” you don’t. You really need energy (ATP derived from oxidation)!
- Eat animal products rare or raw; avoid overcooked animal products since heat destroys essential amino acids (Phe, Lys, Thr, His, Tryp) and valuable enzymes.
*An easy way to calculate the amount is to divide your ideal body weight by 15 to get the number of ounces of cooked meat to be consumed per day. Ex: 150 pound Ideal Body Weight = 10 ounces).