The Patterns of Colon Cancer Appear In The Coagulated Blood

If you have been diagnosed with colon cancer this is what your oxidative mycotoxic coagulated blood looks like with large round and irregular shaped polymerized protein pools in the center moving out to the 2nd and 3rd rings or chakras in this hypocoagulated blood.

If you have NOT been diagnosed with colon cancer and these patterns appear in your coagualted blood then you need to visit your medical doctor immediately for further blood tests for colon cancer.

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The Use of Antibiotics, Probiotics and Enzymes Are Harmful to the Body

The micrographs below show oxidative/mycotoxic stress due to the use of probiotics, antibiotics and digestive enzymes.

The patterns seen in the dried coagulated blood or white polymerized protein pools are also indicative to a pre-cancerous condition of the small and/or large bowel.

The ideal pH of the small bowel is 8.4 free of ALL bacteria. The ideal pH of the large bowel is 7.4 free from all toxic acids, bacteria and yeast.

The use of antibiotics, probiotics and enzymes is based upon an old theory of digestion. The so-called digestive system is now correctly defined as the "alkalizing buffering system" with the ideology that food digests from the inside out once the membranes of the food have been broken with the teeth via mastication.

The mouth secrets alkaline compounds to buffer the enzymes or acids from the food during mastication and the stomach's primary purpose is to alkalize the food ingested NOT digest the food ingested.

The pancreas and the gallbladder along with other glands such as the pylorus glands secret sodium bicarbonate on the food ingested to begin up the pH to 8.4 in preparation of that food chyme to be transformed into stem cells. This biological transformation of the liquid alkalized food ttakes place in the crypts of the small intestine.

The large intestine main purpose is to adsorb and absorb alkalizing minerals and water back into the blood and then eliminate acid residues as solid or liquid waste.

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Obstructive Sleep Apnea Tied To Dr Young's Acid Theory

Obstructive sleep apnea: Intermittent hypoxia leads to sympathetic overactivity and then to atherosclerotic process

Obstructive sleep apnea (OSA) syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep.

Mounting evidence shows that OSA is a risk factor for cardiovascular disease which is supported by epidemiological association studies. Longitudinal cohort studies also provide evidence that patients with untreated severe sleep apnea have an increased rate of cardiovascular events. The prevalence of coronary artery disease (CAD) is 3 to 5 times higher in patients with OSA compared with control populations (1, 2, 3, 4, 5, 6, 7).
Atherosclerosis is recognized as the precursor stage of coronary-myocardial disease.

A very recent paper published in Circulation Journal (8), by far the largest study to date, has showed that moderate to severe obstructive sleep apnea increases the risk of coronary heart disease or death by 68% in men under the age of 70, but does not increase the risk for men over 70 or for women. A total of 1927 men and 2495 women 40 years of age and free of coronary heart disease and heart failure at the time of baseline polysomnography were followed up for a median of 8.7 years in this prospective longitudinal epidemiological study.

Increased carotid intima-media thickness (IMT) and plaque occurrence was reported in OSA patients without any other significant co-morbidity compared to matched controls (9, 10, 11, 12).

The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. The association of OSA and hypertension has additive effects on the development of atherosclerosis. Daytime hypertension develops secondary to the persistently elevated sympathetic state (13). In a recent study of 94 middle-aged patients, the intima-media thickness of carotid artery was positively related to systolic blood pressure and apnea-hypopnea index (14).

Pathophysiological mechanisms linking OSA to atherosclerosis

OSA patients experience intermittent hypoxaemia and CO2 retention that modify the autonomic and haemodynamic responses to sleep (15). Indeed, chronic intermittent hypoxia may lead to sympathetic overactivity (16, 17). A study has shown that with mild apneic events (duration < 20 seconds), pretreatment with 100% oxygen effectively eliminated most of the increase in sympathetic nerve activity (25).

It is interesting to notice that continuous positive airway pressure treatment may reverse early signs of atherosclerosis (18).

There is increasing evidence that intermittent hypoxia is independently associated with dyslipidemia (19). In addition to clinical data, animal experiments also support a role of intermittent hypoxia in the pathogenesis of dyslipidaemia in sleep-disordered breathing (20, 21, 22).

The studies above mentioned confirm old experiments performed on rabbits where oxygen deficiency was attained by placing the animals daily into a chamber with decreased oxygen content (down to 12%) for 3–6 hours, for 4 months. It was shown that prolonged hypoxia brings about a high hypercholesterolemia and greatly intensifies the development of aortic and coronary atherosclerosis (26).

The demonstration that chronic intermittent hypoxia may lead to sympathetic overactivity and dyslipidemia adds more evidence to the acidity theory concept (23), with intermittent hypoxemia joining to other key factors for atherosclerosis, as discussed recently in this blog (24).

Carlos Monteiro

1. Levy P, Pepin JL, McNicholas WT. Should all sleep apnoea patients be treated? Yes. Sleep Med Rev 2002; 6:17–26.
2. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–1053.
3. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al. Ambulatory blood pressure after therapeutic and sub therapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002; 359: 204–210.
4. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365:1046-1053.
5. Unruh ML, Enright PL, Polak JF, et al. The relationship of sleep apnea to carotid wall thickness among a large cohort of older adults. Sleep. 2005;20:A112.
6. Peker Y, Hedner J, Kraiczi H, Loth S. Respiratory disturbance index: an independent predictor of mortality in coronary artery disease. Am J Respir Crit Care Med. 2000;162:81-86.
7 Mooe T, Franklin KA, Holmstrom K, Rabben T, Wiklund U. Sleep-disordered breathing and coronary artery disease: long-term prognosis. Am J Respir Crit Care Med. 2001;164:1910-1913.
8. Daniel J. Gottlieb et al. Prospective Study of Obstructive Sleep Apnea and Incident Coronary Heart Disease and Heart Failure. The Sleep Heart Health Study. Circulation, Published online before print July 12, 2010
9. Drager LF, Bortolotto LA, Lorenzi MC, Figueiredo AC, Krieger EM, Lorenzi-Filho G. Early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 2005; 172: 613–618.
10. Baguet JP, Hammer L, Levy P, et al. The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence. Chest 2005; 128: 3407–3412.
11. Minoguchi K, Yokoe T, Tazaki T, et al. Increased carotid intima–media thickness and serum inflammatory markers in obstructive sleep apnea. Am J Respir Crit Care Med 2005; 172: 625–630.
12. Baguet JP, Hammer L, Levy P, Pierre H, Launois S, Mallion JMv, et al. The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence. Chest 2005; 128: 3407-12.
13. Narkiewicz K, Somers VK. Sympathetic nerve activity in obstructive sleep apnoea. Acta Physiol Scand. 2003;177:385-390
14. Drager LF, Bortolotto LA, Krieger EM, Lorenzi-Filho G. Additive effects of obstructive sleep apnea and hypertension on early markers of carotid atherosclerosis. Hypertension 2009; 53 : 64-9.
15. Somers VK, Dyken ME, Mark AL, Abboud FM. Sympathetic nerve activity during sleep in normal subjects. N Engl J Med 1993; 328 : 303-7.
16. Johnson, T. S., J. B. Young, and L. Landsberg. Sympathoadrenal responses to acute and chronic hypoxia in the rat. J. Clin. Invest. 71: 1263-1272, 1983.
17. Greenberg HE, Sica A, Batson D, Scharf SM. Chronic intermittent hypoxia increases sympathetic responsiveness to hypoxia and hypercapnia. J Appl Physiol 1999; 86: 298–305. Full free text at http://jap.physiology.org/cgi/content/full/86/1/298
18. Drager LF, Bortolotto LA, Figueiredo AC, Krieger EM, Lorenzi-Filho G. Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 2007; 176: 706–712.
19. Drager, Luciano F; Jun, Jonathan; Polotsky, Vsevolod Y. Obstructive sleep apnea and dyslipidemia: implications for atherosclerosis. Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):161-5.
20. Li J, Grigoryev DN, Y e SQ, Thorne L, Schwartz AR, Smith PL, et al. Chronic intermittent hypoxia upregulates genes of lipid biosynthesis in obese mice. J Appl Physiol 2005; 99 :
1643-8.
21. Li J, Thorne LN, Punjabi NM, Sun CK, Schwartz AR, Smith PL, et al. Intermittent hypoxia induces hyperlipidemia in lean mice. Circ Res 2005; 97 : 698-706.
22. Li J, Savransky V, Nanayakkara A, Smith PL. O’Donnell CP, Polotsky VT. Hyperlipidemia and lipid peroxidation are dependent on the severity of chronic intermittent hypoxia. J Appl Physiol 2007; 102 : 557-63.
23. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf
24. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 athttp://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
25. Leuenberger U, Jacob E, Sweer L, Waravdekar N, Zwillich C, Sinoway L. Surges of muscle sympathetic activity during obstructive apnea are linked to hypoxemia. J Appl Physiol 1995;79:581– 8.
26. N. N. Kipshidze.The effect of oxygen deficiency on the development experimental atherosclerosis of the coronary arteries Bulletin of Experimental Biology and Medicine, Volume 47, Number 4, 447-453, 1958, DOI: 10.1007/BF00779624

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Food Reward: a Dominant Factor in Obesity, Part II

How to Make a Rat Obese

Rodents are an important model organism for the study of human obesity. To study obesity in rodents, you have to make them fat first. There are many ways to do this, from genetic mutations, to brain lesions, to various diets. However, the most rapid and effective way to make a normal (non-mutant, non-lesioned) rodent obese is the "cafeteria diet." The cafeteria diet first appeared in the medical literature in 1976 (1), and was quickly adopted by other investigators. Here's a description from a recent paper (2):

In this model, animals are allowed free access to standard chow and water while concurrently offered highly palatable, energy dense, unhealthy human foods ad libitum.

In other words, they're given an unlimited amount of human junk food in addition to their whole food-based "standard chow." In this particular paper, the junk foods included Froot Loops, Cocoa Puffs, peanut butter cookies, Reese's Pieces, Hostess Blueberry MiniMuffins, Cheez-its, nacho cheese Doritos, hot dogs, cheese, wedding cake, pork rinds, pepperoni slices and other industrial delicacies. Rats exposed to this food almost completely ignored their healthier, more nutritious and less palatable chow, instead gorging on junk food and rapidly attaining an obese state.

Investigators have known for decades that the cafeteria diet is a highly effective way of producing obesity in rodents, but what was interesting about this particular study from my perspective is that it compared the cafeteria diet to three other commonly used rodent diets: 1) standard, unpurified chow; 2) a purified/refined high-fat diet; 3) a purified/refined low-fat diet designed as a comparator for the high-fat diet. All three of these diets were given as homogeneous pellets, and the textures range from hard and fibrous (chow) to soft and oily like cookie dough (high-fat). The low-fat diet contains a lot of sugar, the high-fat diet contains a modest amount of sugar, and the chow diet contains virtually none. The particular high-fat diet in this paper (Research Diets D12451, 45% fat, which is high for a rat) is commonly used to produce obesity in rats, although it's not always very effective. The 60% fat version is more effective.

Consistent with previous findings, rats on every diet consumed the same number of calories over time... except the cafeteria diet-fed rats, which ate 30% more than any of the other groups. Rats on every diet gained fat compared to the unpurified chow group, but the cafeteria diet group gained much more than any of the others. There was no difference in fat gain between the purified high-fat and low-fat diets.

So in this paper, they compared two refined diets with vastly different carb:fat ratios and different sugar contents, and yet neither equaled the cafeteria diet in its ability to increase food intake and cause fat gain. The fat, starch and sugar content of the cafeteria diet was not able to fully explain its effect on fat gain. However, each diets' ability to cause fat gain correlated with its respective food reward qualities. Refined diets high in fat or sugar caused fat gain in rats relative to unpurified chow, but were surpassed by a diet containing a combination of fat, sugar, starch, salt, free glutamate (umami), interesting textures and pleasant and invariant aromas.

Although the cafeteria diet is the most effective at causing obesity in rodents, it's not commonly used because it's a lot more work than feeding pellets, and it introduces a lot of variability into experiments because each rat eats a different combination of foods.

How to Make an Obese Human Lean

In 1965, the Annals of the New York Academy of Sciences published a very unusual paper (3). Here is the stated goal of the investigators:

The study of food intake in man is fraught with difficulties which result from the enormously complex nature of human eating behavior. In man, in contrast to lower animals, the eating process involves an intricate mixture of physiologic, psychologic, cultural and esthetic considerations. People eat not only to assuage hunger, but because of the enjoyment of the meal ceremony, the pleasures of the palate and often to gratify unconscious needs that are hard to identify. Because of inherent difficulties in studying human food intake in the usual setting, we have attempted to develop a system that would minimize the variables involved and thereby improve the chances of obtaining more reliable and reproducible data.

Here's a photo of their "system":
It's a machine that dispenses bland liquid food through a straw, at the push of a button. They don't give any information on the composition of the liquid diet, beyond remarking that "carbohydrate supplied 50 per cent of the calories, protein 20 per cent and fat 30 per cent. the formula contained vitamins and minerals in amount adequate for daily maintenance."

Volunteers were given access to the machine and allowed to consume as much of the liquid diet as they wanted, but no other food. Since they were in a hospital setting, the investigators could be confident that the volunteers ate nothing else.

The first thing they report is what happened when they fed two lean people using the machine, for 16 or 9 days. Both of them maintained their typical calorie intake (~3,075 and ~4,430 kcal per day) and maintained a very stable weight during this period.

Next, the investigators did the same experiment using two "grossly obese" volunteers. Again, they were asked to "obtain food from the machine whenever hungry." Over the course of the first 18 days, the first (male) volunteer consumed a meager 275 calories per day. The second (female) volunteer consumed a ridiculously low 144 calories per day over the course of 12 days, losing 23 pounds. Without showing data, the investigators remarked that an additional three obese volunteers "showed a similar inhibition of calorie intake when fed by machine."

The first volunteer continued eating bland food from the machine for a total of 70 days, losing approximately 70 pounds. After that, he was sent home with the formula and instructed to drink 400 calories of it per day, which he did for an additional 185 days, after which his total weight loss was 200 lbs. The investigators remarked that "during all this time weight was steadily lost and the patient never complained of hunger or gastrointestinal discomfort." This is truly a starvation-level calorie intake, and to eat it continually for 255 days without hunger suggests that something rather interesting was happening in this man's body.

This machine-feeding regimen was nearly as close as one can get to a diet with no rewarding properties whatsoever. Although it contained carbohydrate and fat, it did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized. As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a "broken" metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. This also implies that obesity may not be a disorder, but rather a normal response to the prevailing dietary environment in affluent nations.

A second study by Dr. Michel Cabanac in 1976 confirmed that reducing food reward (by feeding bland food) lowers the fat mass setpoint in humans, using a clever method that I won't discuss for the sake of brevity (4). I learned about both of these studies through the writing of Dr. Seth Roberts, author of The Shangri-La Diet. I'd also like to thank Dr. Stephen Benoit, a researcher in the food reward field, for talking through these ideas with me to make sure I wasn't misinterpreting them.

I'd like to briefly remark that there's an anatomical basis for the idea of two-way communication between brain regions that determine reward and those that control body fatness. It's well known that the latter influence the former (think about your drive to obtain food after you've just eaten a big meal vs. after you've skipped a meal), but there are also connections from the former to the latter via a brain region called the lateral hypothalamus. The point is that it's anatomically plausible that food reward determines in part the amount of body fat a person carries.

Some people may be inclined to think "well, if food tastes bad, you eat less of it; so what!" Although that may be true to some extent, I don't think it can explain the fact that bland diets affect the calorie intake of lean and obese people differently. To me, that implies that highly rewarding food increases the body fat setpoint in susceptible people, and that food with few rewarding properties allows them to return to a lean state.

In the next few posts, I'll describe how food reward explains the effectiveness of many popular fat loss diets, I'll describe how this hypothesis fits in with the diets and health of non-industrial cultures, and I'll outline new dietary strategies for preventing and treating obesity and certain forms of metabolic dysfunction.

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Lactic Acid and Hydrochloric Acid (HCL) Cause Atherosclerotic Lesions.

Old experiments with rabbits and dogs provide powerful evidence for the Acidity Theory of Atherosclerosis (1)

Follows a summary about 2 studies from the beginning of the last century showing that acid-fed rabbits and dogs may develop atherosclerotic lesions:

1) Experiments from Oswald Loeb, a well-known professor in pharmacology and scientist from the University of Gottingen - Germany, have demonstrated in study published in 1913, that lactic acid-fed rabbits and dogs have resulted in atherosclerotic lesions in these animals (2). The book “Arteriosclerosis and hypertension, with chapters on blood pressure" (3), by Louis M Warfield, M. D. (Johns Hopkins), showed the following commentary about the experiments from Oswald Loeb:
“Oswald Loeb produced changes in the arteries of rabbits by feeding them sodium lactate (lactic acid). His controls fed on other acids became cachectic, but showed no arterial changes. He further found that in 100 gm. of human blood there was normally from 15 to 30 mg. of lactic acid. After heavy work, he found as much as 150 gm. He considers that after adrenalin or nicotin injections, the function of the liver is so disturbed that lactic acid is not bound. The arteriosclerosis is actually due to the presence of free lactic acid in the circulation. He succeeded, also, in producing lesions of the intima in a dog fed for a long time on protein poor diet, plus lactic acid and sodium lactate.”

2) I. Adler, M.D., from the Laboratories of the New York Board of Health, told in his paper entitled “Studies on Experimental Atherosclerosis” (4), published in 1913, that a casual remark by Dr. P. A. Levene have suggested the simple procedure of adding dilute hydrochloric acid to the dog's food and thus producing a chronic hyperacidity. This led Adler to include acid-fed dogs in his experiments. He told in his paper that though only two dogs have thus far been fed with hydrochloric acid, presenting sclerotic affections, the possibility can not be denied, especially in view of the numerous negative results with other methods, that these positive results are not mere coincidences, but are probably due to the hydrochloric acid. Referring at the end of his paper about the acid-fed dogs presenting atherosclerotic lesions he stated “that the work is being continued, and definite conclusions would at this stage be premature; but perhaps it may be permitted, even now, to venture the statement that in all probability the theory which bases atherosclerosis on a purely mechanical etiology will not prove tenable. Whether mechanical factors come into play at all, and if so, to what extent, remains to be seen. It seems almost certain, at least in our present state of knowledge, influences, subject possibly to more or less nerve control, are dominant factors in the etiology of atherosclerosis. Perhaps it may be discovered also that cholesterin and its various modifications and combinations, while undoubtedly an element of importance in atherosclerosis of the rabbit and human beings, may not be the sole predominant etiological factor.“. He finished telling that “If it should turn out that so simple a procedure as adding a certain proportion of hydrochloric acid to the food of dogs is sufficient to produce lesions of the blood vessels closely analogous, if not wholly identical with human atherosclerosis, a revision of our present theories will become necessary“.

1. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf
2. Loeb, O., Ueber experimentelle Arterienveraender ungen mit besonderer Beruecksichtigung der Wirkung der Milchsaeure auf Grund eigener Versuche, Deutsch. med. Wchnschr., 1913, xxxix, I819
3. Louis M Warfield, M. D., Third Edition, C. V. Mosby Company, 1920, with full free text athttp://www.archive.org/stream/arteriosclerosis00warfuoft/arteriosclerosis00warfuoft_djvu.txt.
4. I. Adler, ‘Studies in Experimental atherosclerosis - A preliminary report’, The Journal of Experimental Medicine, 1913. Free full text athttp://jem.rupress.org/content/20/2/93.full.pdf

Published originally by Carlos Monteiro at http://www.aciditytheory.blogspot.com

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New Scientific Research Confirms Dr Young's Research - Salt Is Good For You!

"All sickness and disease conditions, including all cancers show a deficiency in blood plasma sodium." Dr. Robert O. Young

Salt is GOOD for you: Eating more could even lower the chances of heart disease.

For years, doctors have been telling us that too much salt is bad for us. Until now.

A study claims that cutting down on salt can actually increase the risk of dying from a heart attack or a stroke.

The research has left nutritionists scratching their heads.

Its findings indicate that those who eat the least sodium – about one teaspoon a day – don’t show any health advantage over those who eat the most.

In the eight-year study, people with the lowest salt intake had the highest rate of death from heart disease!

In fact, those with less salty diets actually had slightly higher death rates from heart disease.

The study, which followed 3,681 healthy European men and women aged 60 or younger, for about eight years, also found that above-average salt intake did not appear to increase the danger of developing high blood pressure.

The report, in the latest issue of the Journal of the American Medical Association, was released just three months after the U.S. government launched a public health campaign urging restaurants and food manufacturers to cut down on their use of salt.

Sodium was measured in the urine of those taking part, at the beginning and end of the study.

A little more than six per cent of the participants suffered a heart attack, a stroke or some other cardiovascular emergency during the eight years. About a third of these were fatal.

Those who consumed the least salt had a 56 per cent higher risk of death from a heart attack or stroke compared with those who consumed the most.

This was even after obesity, cholesterol levels, smoking, diabetes and other risk factors were taken into account.

There were 50 deaths in the third of participants with the lowest salt consumption, 24 in the third with medium intake and just ten deaths in those with the highest salt levels.

Lead researcher Jan Staessen, head of the hypertension laboratory at the University of Leuven, in Belgium, said: ‘Our findings do not support a generalized reduction of salt intake in the population.’

The scientists did not have a firm explanation for their results, but they reportedly speculated that low levels of salt in the body could cause more stress in the nervous system, decrease sensitivity to insulin and affect hormones that control blood pressure and sodium absorption.

Read more: http://www.dailymail.co.uk/health/article-1383393/Salt-intake-drop-increase-chances-heart-disease.html#ixzz1LWxcudTM

The Amazing Benefits of Alkalizing Mineral Salts and the New Liquid Salt - pHlavor In my research I have discovered that salt is at the foundation in the creation of all major elements of the body when the elements of oxygen or hydrogen give up their protons. The pathway to magnesium, potassium and even calcium begins with salt. For example, when the protons of oxygen, which are eight, are acquired by the nucleus of the sodium, which is eleven protons, it becomes potassium, which has nineteen protons. The equation is: When potassium acquires an additional proton from the hydrogen ion it becomes calcium or when the sodium ion acquires an additional proton from the hydrogen ion it becomes magnesium. The equations are: It is no coincidence that our body fluids are salted with sodium or that the ocean is salted with sodium rather than some other element. You now have the simple understanding that sodium (salt) is at the foundation of life and without it we would die. This is why I recommend eating more salt in the diet. In fact a 154 pound man or woman should be eating at least 10 grams of salt a day. And when you have sugar cravings it is not the need for sugar it is the need for salt. Eat some salt and your sugar cravings will go away with renewed energy and "sustainable energy"™ Now, just don't eat any salt. It has to be a salt that is whole and unprocessed, free from added iodine or caking agents. I have a salt farm on the north shore of the Great Salt Lake where I harvest the best salt in the world. Shelley and I now have available a new condiment for flavoring your food with a 26% pure sol of salt called pHlavor. You will be amazed when you use this seasoning on your food and how it enhances the flavor of everything you are eating. You no longer need to use acidic condiments of soy sauce, vinegar, miso, tamari, and even Braggs Amino Acids to flavor your food when you have the first alkaline liquid spray salt condiment on the planet - pHlavor™ Let us know what you think as you start eating and enjoying the many benefits of the most important element next to oxygen - SALT in our latest creation called liquid salt pHlavor! To keep our bodies running we need energy - not just any energy but "sustainable energy." To have "sustainable energy" that just keeps going and going and going like the Energizer Bunny you must have salt. Salt is the body's matrix system for transporting energy throughout the entire human organism. A deficiency of salt is equal to a deficiency of energy. You can't even create a thought or move the body without salt. I have discovered that the endocrine system, which includes the pineal gland, the pituitary, hypothalamus, thyroid, adrenals, pancreas and sex glands communicate through a matrix of salt - NOT HORMONES. Hormones are the acidic waste products of the endocrine glands using energy to communicate with each other to maintain homeostasis of the body fluids, energy needs and the autonomic functions of the body. The body needs no hormones - it needs "sustainable energy" that can only be created through a matrix of salt. Interesting Facts About Young pHorever pH Miracle pHlavor Colloidal Mineral Salts 1) Our bodies contain almost 450gms of salt and each day we need to replenish the salt used by our bodies to maintain our normal health, vigor and alkaline design. 2) Salt plays a big part in helping the body to digest food and turn them into living tissues, as well as helping to transmit nerve impulses that contract the muscles. In order for the cells of the body to function normally, a salt/water balance must be maintained. Salt is also necessary for making the sodium bicarbonate the body needs to alkalize the food we eat to maintaining the alkalinity of the blood and lymph fluids. 3) Young pHorever pH Miracle pHlavor colloidal mineral salt tastes great. Minerals present naturally in the salt from the Great Salt Lake North Shore as well as the crystal shape enhances its flavor therefore the salt can be used more sparingly. 4) Young pHorever pH Miracle pHlavor colloidal mineral salt contains higher levels of calcium and magnesium than normal sea or table salts, as these minerals are also naturally present in the Great Salt Lake North Shore water. Some people believe that this balance of minerals has beneficial effects on the body. Certainly we believe these minerals help enhance the taste of the pH Miracle pHlavor colloidal mineral salt - taste it and compare to your current salt. 5) When you are tired and/or fatigued and need energy that is the need for salt. All sugar cravings are the need for salt. 6) Salt is the ion of life in which all energy is transported. Without salt there is no life. 7) Salt is what keeps the spirit body connected or joined with the physical body and mental body. Features and Benefits of Young pHorever pH Miracle pHlavor Colloidal Liquid Salt 1) Young pHorever pH Miracle pHlavor colloidal mineral salt is an evaporated salt that produces a unique three dimensional crystal, it is produced by being very slowly evaporated naturally by the sun, allowing the formation of a 26% concentration of a heterogeneous mineral salt solution. The concentration of this salt is greater then the Dead Sea. 2) It is a very light textured salt with a delicate flavor. The taste is created by the unique crystal size and shape of the Young pHorever pH Miracle pHlavor colloidal liquid mineral salt. 3) Excellent for spraying on top of foods as its light texture means it 'sticks' better - ideal in particular for salting salads and other vegetables! 4) High surface area and low bulk density improves the product adherence. This makes it ideal for spraying on food or in your mouth directly to begin the alkalizing process. The Salt Flush - How to cleanse the Colon easily This process will flush the colon like colonics, just by drinking salt as outlined below: (Very Important: Make sure you have 2 - 3 hours at home when you do this, results happen quickly and you need to allow yourself time to finish the cleansing process). Here's what you do… 1. Do this first thing in the morning on an empty stomach 2. Fill a glass with approximately 4 oz (half full) of warm, good quality water 3. Put in two TEASPOONS of liquid salt and stir the salt in 4. Drink it down in one go 5. Make sure you have plenty of structured water on hand to re-hydrate with as this takes effect

You may also call our office at 760-751-8321 to order this product.

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Jejunal Biopsies of the Small Intestines With Serious Degeneration

These pictures are jejunal biopsies showing serious degenerative conditions of the small bowel and destruction to the intestinal villi. The first picture shows damage to the intestinal villi from several weeks of antibiotics. The second picture shows complete destruction of the intestinal villi from an acidic diet high in animal protein, dairy, grains, and high sugar fruit. The first picture I see in clients with irritable bowel, gas, constipation to diarrhea and Crohn's. The second picture I see in clients with rheumatoid arthritis, atherosclerosis, celiac sprue and colon cancer.

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