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Androgen Deficiency of Aging Male (ADAM) and Hormone Replacement

Dr. Renata Trister DO

Male hypogonadism, or testosterone deficiency syndrome (TDS), results from a failure of the testes to produce adequate androgen. Patients have low circulating testosterone in combination with clinical symptoms such as fatigue, erectile dysfunction and body composition changes. The cause may be primary (primary testicular failure due to genetic anomaly, infection, chemotherapy/radiation) or secondary (defect in hypothalamus or pituitary), but often presents with the same symptomatology. In the older patient, androgen deficiency of the aging male (ADAM) is an important cause of secondary hypogonadism because testosterone levels decline progressively after age 40. Hypogonadal patients have alterations not only in sexual function and body composition, but also in cognition and metabolism. Regardless of the cause, hypogonadal patients who are both symptomatic and who have clinically significant alterations in laboratory values are candidates for treatment. The goal of hormone replacement therapy in these men is to restore hormone levels to the normal range and to alleviate symptoms suggestive of hormone deficiency. This can be accomplished in a variety of ways, although most commonly testosterone replacement therapy (TRT) is employed.

Androgen deficiency of the aging male (ADAM) is a cause of secondary hypogonadism that often goes unrecognized. This phenomenon of hypogonadism due to aging has also been described as testosterone deficiency syndrome, late-onset hypogonadism, and andropause. Symptoms of this condition resemble those of ‘normal’ aging and include changing body composition (osteopenia, increased adiposity, decreased muscle mass), decline in energy and stamina, decreased cognitive function, decreased libido, and erectile dysfunction. On a metabolic level, men with lower androgen levels have demonstrated higher glucose and insulin levels, higher rates of obesity, and an increased incidence of type 2 diabetes. Several studies have shown a significant improvement in insulin sensitivity in diabetic men treated with supplemental testosterone. Studies have also suggested a link between hypogonadism and cardiovascular disease, which is not surprising given the relationship with hypogonadism and  metabolic syndrome. Testosterone levels in men begin to decline in the late third or early fourth decade and diminish at a constant rate thereafter.

Validated questionnaires have been developed to assess symptoms associated with androgen deficiency, such as the ADAM questionnaire and the Aging Male Survey.

Androgen Deficiency of the Aging Male (ADAM) Questionnaire. The ADAM questionnaire is considered positive if the patient answers ‘yes’ to questions 1 and 7, as well as two to four of the other items [Morley et al. 2000].

1.Do you have a decrease in libido or sex drive?

2.Do you have a lack of energy?

3.Do you have a decrease in strength and/or endurance?

4.Have you lost weight?

5.Have you noticed a decreased ‘enjoyment of life’?

6.Are you sad and/or grumpy?

7.Are your erections less strong?

8.Have you noticed a recent deterioration in your ability to play sports?

9.Are you falling asleep after dinner?

10.Has there been a recent deterioration in your work performance?

Many positive responses in the questionnaire may be indicative of other conditions such as depression. It is therefore important to combine the results of these questionnaires and laboratory measurements of androgen levels and other clinical symptoms to formulate a diagnosis of hypogonadism.

Once the diagnosis is established, several methods of testosterone replacement treatment (TRT) are available. The goal of hormone replacement therapy in hypogonadal men is to restore hormone levels to the normal range of young adult males and to alleviate symptoms suggestive of hormone deficiency. Restoration of normal testosterone levels with replacement therapy can improve muscle mass, prevent osteoporosis, maintain mental acuity, and restore libido, especially in elderly males. While these benefits of TRT in hypogonadal men are well described, not all hypogonadal patients receive only testosterone as a means of hormone replacement. In general, treatment is either in the form of direct androgen replacement with testosterone therapy, or in the form of replacement of pituitary gonadotropins to stimulate endogenous androgen production. Treatment of hypogonadism needs to be tailored to the underlying cause. Since most men over the age of 50 have declining levels of testosterone (a so-called ‘relative hypogonadism’), such men should only be considered candidates for hormone therapy if they have clinical manifestations of ADAM in addition to low testosterone.

TRT modality

Dosing regimen

Intramuscular injection Testosterone enanthate/cypionate: every 2-3 weeks
Transdermal gels/patches Androderm: 5mg/day
Testoderm: 40cm2 scrotal patch (1 patch/day)
Gels (Testim/Androgel): 5–10mg/day
Subcutaneous pellets Testopel: 75mg pellets; 6–12 pellets (450–900mg) Q3–6 months




Gastrointestinal Physiology

By Jon Trister, MD

Gastrointestinal Physiology.
It is important to understand GI function.

Neurological consideration.
Glossopharyngeal nerve (Cranial nerve IX): mixed, sensory and motor nerve.
Sensory function:Oropharynx,Eustachian tube,Middle ear,Posterior third of the tongue,Carotid sinus, Carotid body, Taste to posterior third of the tongue, Supplies parasympathetic fibers to the parotid gland via otic ganglion,contribute to the pharyngeal plexus.
Motor function: Stylopharyngeus muscle.

Vagus nerve (Cranial nerve X):
a)Parasympathetic control of the heart, lungs, gastrointestinal tract.
b)Sympathetic control of the peripheral chemoreceptors.
Dorsal nucleus of the vagus nerve:Parasympathetic output to the intestines;
Nucleus ambiguus:Parasympathetic output to the heart;
Solitary nucleus:Receives afferent taste information and afferent info from visceral organs.
Spinal trigeminal nucleus:afferent impulses arising from the outer ear, the dura of the posterior cranial fossa and mucosa of the larynx.

Accessory nerve ( Cranial nerve XI):Originates in the C1-C2 segments): Innervates sternocleidomastoid and trapezius muscles.
It enters the scull via foramen magnum, travels along the inner wall toward jugular foramen and leave the scull again fia Jugular foramen together with IX and X nerves.

Cranial nerves IX-X-XI provide neurological regulation of the gastrointestinal function.
They pass through jugular foramen which has very complex anatomy.JUgular foramen is formed by the anterolateral part of the temporal bone and posteromedial part of the occipital bone.
Its subdivided into larger posterolateral compartment ( pars venosa) containing the jugular bulb and tenth and eleventh cranial nerves and a smaller anteromedial compartment ( pars nervosa) containing the ninth cranial nerve.These two parts are usually separated by a fibrous bridge connecting the jugular spine of the petrous temporal bone to the jugular process of the occipital bone.This bridge could be osseos or fibrous.
Size of the right jugular foramen is usually larger than the left.
Dura over the jugular foramen had a two perforations forming a glossopharyngeal meatus through ninth nerve passed to enter the pars nervosa and vagal meatus through which vagus and accessory nerves entered the anteromedial part of the pars venosa and jugular bulb.The glossopharyngeal and vagal meati consistently separated by a dural septum.(Albert Rhoton etc, J.Neurosurgery/Volume 42/May 1975).

This complex anatomical entity is a subject to somatic dysfunction as the result of trauma, congenital abnormalities, tumors,dural strains, inter- and intraosseous strains of the temporal and occipital bones.
Those pathologies may alter anatomical relationship of the structures occupying the jugular foramen and subsequently to their physiological dysfunction.

Digestion begins with imaginary stimulation: thinking , seeing and smelling food send signals to the brain via afferent nerves. In the brain processing of information is occurs and efferent pathway-parasympathetic- glossopharyngeal nerve is activated to stimulate salivary glands to produce saliva rich in digestive enzymes-amylase ( initial breakdown of carbohydrates) and lipase (initial breakdown of triglycerides).
Glossopharyngeal nerve ( IX)
[originates in upper medulla, passes through the Jugular foramina]: Stimulate salivary glands.
Vagus (X) [Originate in medulla oblongata and passes through the Jugular foramina] Control digestive tract from the esophagus to the mid-colon.
Accessory nerve (XI) [Originate at the junction of medulla oblongata and spinal cord and passes via jugular foramen with IX and X nerves]
1.Mastication stimulates production of the saliva by oral salivary glands (IX).Mastication stimulates gastric secretion of Pepsin and water (X). 
Stomach:Distention of the esophagus stimulates the oral salivary glands.Distention of the gastric fundus stimulates secretion of the Pepsin,HCL, Intrinsic Factor and water.
Distention of the antrum stimulates Gastrin secretion. In addition, the cells lining the stomach secrete a thick mucus coating that protects the stomach from acid and pepsin.
Distention of the duodenum stimulates secretion of the Pepsin, HCL, Intrinsic Factor and water. Pepsin is active in acidic environment. Pepsin is very specific in digestive capability: it break down only [protein linkages containing certain amino acids : tryptophan , tyrosine, Methionine and leucine.
The presence of food stimulates the vigorous contraction of the muscles of the stomach wall, mixing of the food particles with digestive juices and push semi digested food into duodenum.
Antral drainage inhibit secretion of the  Pepsin, HCL, Intrinsic Factor and water

Gastrin amplifies antral production of the HCL, Intrinsic Factor, Pepsinogen and water
Gastrin amplifies duodenal secretion of Cholecystokinin
Gastrin is produced by G cells of antrum, in the duodenum, small intestine and pancreas.
HCL inhibit production of Gastrin.HCL stimulates secretion of Secretin by duodenum
Duodenum very complex process and regulated by nervous system and hormones:
Gastrin stimulate the formation of the Cholecystokinin.Lipids in the jejunum stimulate secretion of the Cholecystokinin.Carbohydrates and HCL in duodenal bulb stimulate secretion of the Cholecystokinin.Cholecystokinin induce gallbladder contraction and opening of the hepato-pancreatic ampulla.
Cholecystokinin stimulates production of the Insulin, HCO3, Glucagon in the pancreas
Cholecystokinin inhibit antral secretions and bulbar acidity.Secretin reduce HCL production and stimulate HCO3 production by pancreas which protect duodenal bulb from acid.Secretin stimulate Insulin release and inhibit Glucagon release.Duodenum also secretes mucus for protection from destructive effect of HCL.
Hypertonic Glucose solutions, Acidity in the bulb, Lipids in the jejunum limit the formation of the HCL and diminish gastric motility.If Lipids, proteins and carbohydrates evacuated at the same time disturbing of digestive function might occurs.
Enterokinase in duodenum convert into Trypsin and inhibit Action of the biliary salts.Biliary salts (weak concentration) stimulate Lipase secretion and inhibit (strong concentration) Lipase secretion. 
Gastrin Stimulates: HCL and Water secretion by stomach; secretion of Pepsin, Secretion of Intrinsic Factor, Secretion of Cholecystokinin in the duodenum.
HCL: Inhibits secretion of Gastrin; Stimulates secretion of Secretin; Stimulates production of pepsin from pepsinogen.Anti-bacterial function; Converts Ferric iron to Ferrous iron(absorbable)
Cholecystokinin: Stimulates action of biliary salts, Contraction of Gallbladder, dilatation of choledocho-pancreatic ampula,inhibit gastrin and HCL production; stimulates HCO3, insulin and glucagon release
Secretin: Inhibit HCL, Glucagon, stimulate Insulin release ,stimulates HCO3 production by Pancreas

Endocrine function:
Alpha cells produce and secrete Glucagon, which pancreas release in response to low blood sugar in the serum.Glucagon stimulates breakdown of glycogen ( liver and muscles) to glucose , which is released into bloodstream to serve as a source of cellular energy.
Beta cells secrete insulin in response to high glucose level in the serum.Insulin ( among other functions) drive glucose into muscles and liver to store in the form of glycogen.
Delta cells produce and secrete somatostatin , a complex hormone that is also produced by intestinal lining cells as well as certain neurons in the brain.In the pancreas somatostatin can inhibit release of insulin and glucagon (!?!) to help maintain blood sugar level in a very narrow range.

Exocrine function:
The cells of exocrine pancreas arranged in acini- special clusters along the network of channels forming pancreatic duct-to secrete pancreatic enzymes.
Proteolytic enzymes:Trypsin, Chymotrypsin, Carboxypeptidase A, Carboxypeptidase B,Elastase, Amynopetodases, Dipeptidases, Tripeptidases,Pepsin.

Each of these enzymes has precise and specific function.
Trypsin will break down a protein only at amino acid linkages containing either arginine or lysine.
Chymotripsyn will break down a protein at amino acid linkages containing tryptophan,phenylalanine, tyrosine.
DIpeptidase will break down a protein consisting two amino acids
Tripeptidase will break down a protein consisting three amino acids
All of these enzymes are produced in in-active forms to prevent self-destruction:
Trypsinogen, Chymotripsynogen,Procarboxypeptidase,Prodipeptidases,Protripeptidases
The acing cells also secrete multiple lipases and amylases.
The acinar cells store the inactive precursors in little sacs, or vacuoles, in the cytoplasm, until they are needed for digestion.As ling as these pre-enzymes remain in their inactive form, they pose no threat to the pancreas themselfs.
The body has a remarkable mechanism for signaling the acinar cells of the pancreas to begin manufacturing and secreting stored precursor enzymes.
First, the presence of the food in the mouth and in the stomach stimulate vagal nerve to release its neurotransmitter-Acetylcholine which stimulate release of pre-enzymes into the common space of cul-de-sac.
The presence of food in duodenum stimulates lining cells of duodenum to secrete the hormone Cholecystokinin into bloodstream. This hormone like vagus nerve stimulates the acinar cells to produce and release stored enzymes into duct of Wirsung and than empty pre-enzymes into the duodenum via Vater papilla.
The cells lining the small intestine produce proteolytic enzyme calle enteropeptidase, whose function is specifically to cleave off the six-amino-acid tail of trypsinogen, leaving the active and very powerful trypsin.
Trypsin activates other proteolytic enzymes making them active, to digest protein-cascade reactions.
This semiliquid food boluses that make their way from the stomach to intestine are extremely acidic, from stomach HCL.But Trypsin and Chemotrypsin can perform their digestive function only in an alkaline environment.To solve this problem, lining cells of small intestine sense the load of incoming food, they release another hormone, Secretin into the bloodstream.Secretin stimulate pancreas to produce NaHCO3, powerful antacid quickly neutralizes acid produced earlier by stomach.Now, the activated Enzymes have an ideal environment in which to begin digestive work.


Clinical, biomechanical and pathological correlation in Orthopaedic Medicine

Physicians practicing Orthopaedic Medicine must be able to utilize different clinical findings for identification of the pathological processes.

Restriction of the ROM, pain, changes in the texture of the structures, autonomic manifestations ( sweating, temperature, color changes, etc) will indicate the involvement of different structures in the pathological process. All of these processes indicate disruption of Bio-tensegrity.

I will present several examples:


Entrapment of the sciatic nerve may occur at various areas along its course and may be difficult to differentiate from a herniated disc.Detailed history and examination may give a clue  to the source of the problem.In most cases, sciatica develops at the area of pelvic musculo-tendinous junction.
Piriformis syndrome is an example of the above.
The sciatic nerve may have a high division and may pass through the Piriformis muscle.
In such cases compression of the nerve by surrounding musculature may give rise to neuropathy.
The following muscles can contribute to the symptoms of “Sciatica”
Attachments:Sacrum & greater trochanter.Function: lateral rotation.Innervation : L5-S1S2
Quadratus femoris.Attachments: Ischial tuberosity & intertrochanteric crest
Function: lateral rotation
Innervation:L4-L5-sacral plexus
Gemelli inferior.
Attachments: Ischial tuberosity &
Obturator interns tendon.Function:lateral rotation.Innervation:L4-L5
Gemelli superior.
Attachments: Ischium spine & Obturator interns tendon
Function: lateral  rotation
Obturator internus.
Attachments: Ischiopubic ramus & Greater trochanter.Function: Lateral rotation
Inneravation: L5-S1-S2
All of the above muscles go into contractual state as the result of ligamental instability of the pelvic ligaments: the most important include: sacro-iliac , sacro-tuberous, ilio-lumbar  ligaments, as well as the posterior ligamentous and tendinous structures of the hip.
Clinical symptoms of muscular involvement/ compensation will be pain, restricted mobility and external rotation of the leg.
Ligamental relaxation develop as the result of various etiologies including: trauma, overuse, metabolic /infectious processes resulting in muscle contractures. (Clinical manifestation of the ligamental laxity and examination pearls described in details in G.Hackett Prolotherapy text).
This lead to compression of the neighboring  neuro-vascular structures by the muscles and tendons: initially only capillary network, leading to chronic ischemia of the corresponding nerves and later to compression of the nerves with symptoms of neuropathy.
Fascial distortion leads to fascial shifts and mechanical injury of the cutaneous nerves and neurogenic inflammation.Contractures of surrounding musculature are secondary to ligamental laxity of the joint leading to a decrease in range of motion of the corresponding joints, which are “aiding” in its stability.
The major concept of Prolotherapy and Orthopaedic medicine is stabilization of the joints via restoration of the ligaments. This will lead to restoration of muscle, blood flow, & nerve decompression thereby restoring its function.In the case of sciatica the targets of Prolotherapy will be Ilio-lumbar, sacroiliac, sacro-tuberous, sacro-ischial ligaments and posterior hip capsule.
Osteopathic manipulative therapy may facilitate normal anatomical realignment .
Peri-neural subcutaneous injection of the D5W (Neuroprolo) will help to reduce neurogenic inflammation and restore fascial distortion.Acupuncture will also assist in regulation of the viscera-somatic aspects of ligamental laxity.Similar principle will be applicable in the other anatomical areas:
Lateral elbow pain:
Laxity of the annular radial ligament and resulting increase in superior translation of the radius  will lead to compensatory spasms and contractures of the proximal forearm muscle; the most important-supinator.
These will lead to compression of the posterior interosseous nerve at the Arcade of Frohse.
Thoracic outlet syndrome in some cases is a manifestation of ligamental laxity. It occurs as a result of abnormal  muscle tone, postural changes, and compression of the neurovascular structures.
These examples indicates the importance of the  meticulous clinical examination and imaging studies for confirmation of the possible pathological processes.
Orthopaedic medicine is a life long affair. Please, be persistent and patient.

Jon Trister MD


Cholesterol Conundrum

By Renata Trister, DO

Most people who are even a little bit concerned about their cholesterol know that there is a“good/Healthy cholesterol” – known as HDL, and a “bad/Lousy cholesterol”  – known as LDL. Although, research shows that the higher the amount of HDL and the lower the amount of LDL in the blood, the less likely a person is to suffer a heart attack or stroke, the “causal” relationship between cholesterol and these illness has not been determined.  Roughly one in six Americans with “unhealthy” cholesterol levels. In the past 15 years, prescriptions of cholesterol lowering medications has soared.  In 2011, 260 million prescriptions were dispensed in US alone.


Scientific opinions differ on cholesterol issues, and there is contrary evidence to theories. Two major clinical trials in the past three years have greatly complicated the picture. The first study, from 2008, shows that lowering LDL levels does not always decrease the risk of having a heart attack. Similarly, results from the second study, show that raising HDL levels does not always translate into fewer heart attacks or strokes. These perplexing findings do not mean that people should stop taking their cholesterol medications. The results have, however, underscored the danger of indulging in a common logical shortcut – assuming that artificially producing normal test results in a patient is the same as conferring good health on that patient. For one thing, drugs typically do not mimic normal conditions perfectly. For another, heart attacks and strokes occur after a complex series of processes that may take years to unfold. Simply altering one of these processes does not necessarily fix the whole problem.

Understanding Cholesterol Testing and its Functions.

Cholesterol is a crucial building material in the body. It helps maintain the structure of cells and vessels, improving overall health and function in the body.


About 80% of cholesterol is produced in the body. Liver, brain and other cells produce cholesterol. About 20% of cholesterol comes from food.

The cholesterol screening test that is usually performed is a blood test called a lipid profile. Results of a lipid profile will come in the forms of numbers. The values of LDL, HDL, trigycerides and total cholesterol are measured.

There is no such thing as “bad cholesterol”.

HDL and LDL are actually proteins that carry cholesterol. Cholesterol can’t dissolve in the blood (like oil and water). It has to be transported to and from the cells by carriers called lipoproteins – HDL, LDL.  These carriers have different and crucial functions, they are not “good” or “bad”. Low-density lipoprotein, or LDL carries cholesterol made in the liver to other tissues.  The liver synthesizes cholesterol based on need. High-density lipoprotein, or HDL carries cholesterol from peripheral tissue back to the liver.

The following is a few vital functions of cholesterol:

–        Cholesterol is a precursor to important sex hormones like testosterone, estrogen, androgen and progesterone. It is also a precursor to corticosteroids, hormones whose primary function is to protect the body against stress and disease.


–        Used as an insulator around nerves, cholesterol is absolutely essential for brain function.


–        Bile salts are made from cholesterol, adequate cholesterol is needed for proper digestion.


–        Cholesterol is a precursor to vitamin D, an important nutrient which supports a healthy immune and nervous system, reproduction, insulin production and the metabolism of minerals.


–        Serotonin receptors in the brain require cholesterol in order to function properly. Serotonin is an important neurotransmitter, low levels of serotonin are linked to depression.




Triglycerides make up about 95% of your body’s fat and are the chemical form in which most body fats exist. The fat produced from triglycerides is used for energy production, provides your body’s organs with insulation, and is a central component in the structure of cell membranes.  Unused triglycerides are transferred to fat cells for storage.  When energy is needed, hormones can cause the release of the stored fats.  Excess triglycerides increase the risk of stroke, heart attacks, fatty liver, pancreatitis and obesity.


Since triglycerides are part of a serum lipid blood test, and lipids are fats circulating in the blood, most people assume high fat diets increase triglycerides.  They are surprised to learn sugars, refined grains, and fruit sugars cause elevated triglycerides.


High blood sugar levels lead to high triglycerides levels. Sugars and refined grains stimulate insulin production.  Insulin stimulates the liver to produce triglycerides. Triglycerides in the blood are not made from dietary fats but made in the liver from excess sugar, which has not been used for energy.  Eating more calories than your body can use for energy contributes to higher triglycerides.


Vascular Damage  

The LDL cholesterol is made in response to damage and stress. When blood vessels are damaged, LDL-carried cholesterol “patches up” the arterial lining with a buildup of fatty material, or atherosclerotic plaque. Much of the time the plaque stabilizes without creating too many immediate problems, but sometimes it bursts, triggering blood clots that lead to heart attacks and strokes if the clots prevent blood from delivering critical oxygen to heart or brain tissue. Without oxygen, the affected tissue dies.

People with high LDL levels may form arterial plaques that are more likely to burst. Some people develop extremely high LDL levels because of a genetic disease called familial hypercholesterolemia that severely limits their ability to clear cholesterol from their blood. They suffer heart attacks in their thirties or forties, which is several decades earlier than the average for the general population. On the positive side, those who maintain normal cholesterol levels (LDL less than 100 milligrams per deciliter of blood and HDL cholesterol levels greater than 40 mg/dL) throughout their life without medication are much less likely to suffer heart attacks or strokes.

A Shortcut ?

With all this evidence linking heart disease to cholesterol levels, it is no wonder that researchers in general and pharmaceutical companies in particular reached a fairly straightforward conclusion: anything – such as a medication – that reduces LDL levels and raises HDL levels must also reduce heart disease risk. By the 1980s the drug industry began marketing a whole family of cholesterol-lowering drugs called the statins, which work by blocking a liver enzyme that is essential for forming cholesterol. Clinical studies proved that statins do in fact reduce the number of heart attacks in people with high cholesterol.  Might statins provide benefits unrelated to cholesterol reduction? There is some evidence that they also decrease inflammation. (When inflammation occurs in the arteries, it is thought to increase the risk of heart disease.) A 2008 study called the JUPITER trial tested statins in about 18,000 people with normal LDLs but elevated C-reactive protein, a measure of inflammation. Statins reduced the risks of heart attack and stroke. That led proponents to conclude that by working through an additional mechanism—lowering inflammation, not just LDL—statins were helping even people with normal LDL levels. Cholesterol lowering drugs also have anti-inflammatory properties Inflammation is strongly suspected of contributing to atherosclerosis.

To some extent, as long as the statins were working, few people worried too much about why they were helping. But statins are not for everyone. Some people cannot tolerate the drugs’ multiple side effects, including muscle pain and, more rarely, liver damage. Others cannot lower their LDL levels enough simply by taking a statin. In addition, at least one in five people whose LDL levels are well controlled by their medications still experience heart attacks or strokes.

Food and Lifestyle:


Elevated blood cholesterol may be a response to stress and injury (damage repair, cell formation, hormones production…). Trans fats, refined sugars, artificial sweeteners, industrial meats, genetically modified foods can cause total and LDL cholesterol rise because they stress and injure tissues. Therefore, diet and lifestyle changes can be very beneficial.

Weight loss. Even a modest amount of weight loss can lower cholesterol levels.

Reduce the amount of sugar and flour in your diet. Recent evidence indicates that added sugar – in the form of table sugar (sucrose) or high-fructose corn syrup – is probably a greater contributor to heart disease than is consumption of saturated fat. This suggests that the inflammatory hypothesis may in fact have more validity than the conventional lipid hypothesis, although the debate is far from settled. As a general rule, avoid processed sugars, particularly soft drinks and highly processed snack foods, which can cause rapid spikes and dips in blood sugar levels. The result can be overeating, obesity and heart disease.

Avoid trans-fatty acids.

These heart-damaging fats can reduce HDL (“good”) cholesterol levels and raise levels of LDL (“bad”) cholesterol. The tip-off that trans-fatty acids are present in foods is the listing of “partially hydrogenated oil” on a food’s ingredient list. Trans-fats are found in many brands of margarine and in most heavily processed foods, as well as in snack foods such as chips, crackers and cookies, and in the oils used to cook fast-food French fries, doughnuts and movie popcorn.

Decrease toxic load by eating fresh organic foods when possible.

Exercise. Daily aerobic exercise can help increase HDL levels.

Don’t smoke. Smoking itself is a risk factor for heart disease. It can also significantly lower HDL cholesterol.

Stress. Emotional stress may prompt the body to release fat into the bloodstream, raising cholesterol levels.