Healthy Weight Maintenance

Healthy Weight Management

We use various approaches in helping our patients to achieve and maintain healthy weight. The following information may help you to get better idea what and how we do it.

ALCAT

The Effect of The ALCAT Test Diet Therapy for Food Sensitivity in Patient’s With Obesity.
(Article from Middle East Journal of Family Medicine)

The ALCAT test uses a specially designed particle counter (hematology analyzer with an automated assay sampler) and food test agents to semi-qualitatively measure white blood cell reactivity, if any, to each agent analyzed. The degree of reactivity is determined by comparing a baseline distribution curve (of the white cells) against the distribution curve generated by the analysis of each test agent/blood sample, and calculating the absolute differences between the curves and the standard deviation (SD). Any reactivity under SD1 will be considered as non-reactive (NEG); reactivity between SD1 and SD2 will be considered as marginally reactive (RANGE 1+); reactivity between SD2 and SD3 will be considered reactive (RANGE 2+); and finally, reactivity above or equal to SD3 will be considered markedly reactive (RANGE MPOS).
There is evidence demonstrating the ALCAT test to be effective in improving body mass index (BMI) and/or scale weight. According to a Baylor University study, “As compared to following a plan of their own choosing, participants who followed the ALCAT plan achieved rather dramatic changes in their body composition.” This experiment showed that 98% of the subjects following the ALCAT plan either lost scale weight or improved their body composition.(11)Dr. J.R. Cabo-Soler, Chief of Biochemistry at the University of Valencia, reported that iso-caloric food elimination diets, based on ALCAT test results, promoted enhanced weight loss, comprised more of adipose tissue, rather than muscle mass, as determined by DEXA studies in a population of refractory weight loss subjects.(12) The ALCAT test has demonstrated a reproducibility of 94.94%, according to a trial by Steinman et. al at the University of Cape Town.(13) 92.0678% reproducibility was reported by Neetling et. al. at the University of the Free Orange State, also in South Africa, which makes it an acceptable screening model for intolerance testing in humans. In Addition, a Norwegian study reported the ALCAT test to be >90% reproducible.(16,14)Fell et. al reported an 83.4% correlation between ALCAT test results and double blind oral challenges as determined by careful clinical evaluation in statistically significant number of patients exhibiting food sensitivity related symptoms, such as migraines, irritable bowel syndrome, eczema and other conditions, that are often observed as co-morbidities in obese patients.(15)
Despite mounting evidence of the efficacy of the ALCAT test in reducing obesity and the overall activation of the immune system, there have been no studies of the weight loss benefits of the ALCAT test reported for an Arab population. The purpose of this study was, therefore, to determine the effectiveness of the ALCAT test as a weight loss tool in
Arab patients who had experienced difficulty achieving goal weight by calorie restriction.

Table 5: The Body Mass Index of 27 patients before and after 12 weeks of following the ALCAT diet plan.

Patient No	Sex	Age (years)	Height (cm)	BMI {weight (kg)/ height (m2)
Patient No	Sex	Age (years)	Height (cm)	Before	After
1	M	46	165	33.1	27.5
2	F	40	167	28.7	21.5
3	F	41	169	29.1	24.5
4	M	40	171	35.2	28.7
5	F	43	170	36.7	26.3
6	F	39	170	33.2	27.0
7	F	48	172	25.7	20.3
8	M	42	169	24.9	22.4
9	M	40	168	30.5	24.8
10	M	33	165	32.7	25.7
11	M	43	167	33.3	27.6
12	F	40	170	29.1	23.5
13	F	45	168	31.9	26.2
14	M	49	173	28.4	24.4
15	M	51	167	34.4	28.0
16	F	53	171	38.3	29.1
17	M	48	170	35.6	29.8
18	M	56	169	33.6	28.0
19	M	40	170	28.0	29.1
20	F	43	165	30.1	29.8
21	F	34	169	30.1	28.0
22	M	30	170	30.8	23.2
23	F	46	168	33.0	25.7
24	M	50	167	37.3	24.9
25	M	43	166	39.9	26.3
26	F	38	168	35.4	28.3
27	F	34	170	27.7	23.2
Mean +SD		42.77 +6.23	168.66 +2.09	32.1 + 3.8	26.1 + 2.63

http://www.mejfm.com/mejfmApr09_vol7-iss3/alcat.htm

Proper diagnosis and treatment of the underactive thyroid gland

Many people suffer from the symptoms associated with hypothyroidism. Some actually have this condition in a form that a doctor is likely to identify; some have unrelated conditions that can look like hypothyroidism but the majority have a condition referred to as subclinical hypothyroidism. This refers to a situation where the lab numbers are not out of range but they reflect a level of dysfunction significant enough to cause symptoms. Unfortunately, most health practitioners will not identify a thyroid problem unless the numbers are outside of the reference range.

Symptoms of Hypothyroidism

· Fatigue
· Weakness
· Weightgain or increased difficulty losing weight
· Coarse, dry hair
· Dry, rough pale skin
· Hair loss
· Cold intolerance (can't tolerate the cold like those around you)
· Muscle cramps and frequent muscle aches
· Constipation
· Depression
· Irritability
· Memory loss
· Abnormal menstrual cycles
· Decreased libido

It is very important to be an educated patient and to know what lab values may suggest that your thyroid function is not optimal even if your current doctor is not recognizing it. I have seen many people who have been told that their thyroid numbers were fine despite having symptoms of low energy, weight gain, hair loss and depression. Invariable they were recommended to start anti-depressant medication. Upon further investigation and more detailed thyroid studies it was clear that their symptoms were more related to low thyroid function rather than from a true case of depression.

Understanding the lab tests:

Standard lab tests for thyroid function include TSH, T4 and T3 uptake. Although these can be valuable, there are more specific tests that better reflect how thyroid function is affecting your health and metabolism. The best thyroid test combination for most people is a TSH, Free T4 and Free T3.

TSH:

The TSH is a measure of how much your body desires thyroid hormone. When the TSH is too low the body is telling us that it wants the thyroid to back off of hormone production. This most often occurs when people have overactive thyroids (hyperthyroidism). If the TSH is elevated, we know that the body is asking the thyroid to do more work and produce more hormones. The TSH will be elevated in hypo-thyroidism because a sluggish thyroid will have trouble keeping up with adequate hormone levels. The technical reference range for TSH on lab work is from 0.5-5.5. Usually as long at it falls in that range doctors will give you the stamp of approval. However, there is a range I refer to as the "optimal range" which is a reflection of where the TSH should be if your thyroid gland is working in a manner that produces optimal metabolism and physiologic function. This optimal range is very narrow and exists between about 1.2 and 2.2 for TSH. This information is based on rigorous clinical trials. In publishing new clinical guidelines in 2002, the American Association of Clinical Endocrinologists fairly dramatically formalized a reversal of its previous doctrine, establishing a narrower "normal" TSH margin of 0.3–3.0. If your TSH is above 2.2, and certainly if it is above 3 you very likely have subclinical hypothyroidism.

Free T4:

T4 is the main thyroid hormone, consisting of 99% of circulating hormone. The word "free" indicates that it is being measured in it’s free state vs. it bound state. All hormones in the body must travel around bound to protein carriers. In the bound state they are inactive. It is only once the hormone has been released from its carrier that it has the capability to influence cellular activity. By measuring free hormone levels we get an accurate representation of the amount of thyroid hormone actually available to benefit our cells. Estrogen and testosterone imbalances, stress, nutritional deficiencies and genetics can all determine how much hormone is free and how much is bound. Like TSH, Free T4 also has narrow optimal range. Most practitioners skilled in working with subclinical hypothyroidism like to see Free T4 levels between 1.2 and 1.3.

Free T3:

T4 is technically classified as a pre-hormone and must be converted into its activated counter-part in order to turn on cellular metabolism. The activated counter part is T3 which represents only about 1% of circulating thyroid hormone. Don’t be fooled by its low circulating percentage, T3 is 99% more biologically active than T4 when it comes to actually stimulating metabolism. Again, we are measuring the “free” hormone as this is the only one we are interested in when assessing actual hormonal influences on our cells. Optimal range for free T3 is 3.3 or depending on the measuring unit 330.

One of the most important factors in subclinical hypothyroidism is the ability of an individual to effectively convert T4->T3. If this process is hindered significantly it will result in presentation of hypo-thyroid symptoms as there is a reduction in the amount of active hormone being produced. The most common reason for poor T4->T3 conversion is a simple nutritional deficiency and can easily be corrected. Selenium, zinc and B6 are the most common nutrients associated with improving conversion capability.

This is the hardest form on subclinical hypothyroidism to pick up because the TSH and the T4 often look totally normal. Due to the fact that most practitioners only measure TSH and T4 the thyroid picture will look totally normal. Free T3 levels are very rarely ordered on routine blood tests mainly because they are thought to be expensive. However, with recent advances of lab technology Free T3 levels are very affordable and easy to acquire. Many practitioners rely on the T3 uptake test to asses T3 levels not realizing that T3 uptake is a test designed to measure T4 levels. Ninety five percent of thyroid screens done in this country never measure T3 levels and thus never assess the levels of active thyroid hormone.

If you have symptoms of hypo-thyroidism it is important to make sure that all the appropriate lab tests are done and interrupted in the correct way. It is best to assume that your practitioner is not familiar with subclinical hypothyroidism so it will be your job to adequately educate them about what lab tests you would like and why.

Low testosterone = abdominal fat gain

As it turns out, there is a scientific explanation for the tendency toward abdominal obesity among middle-aged men. As men age, their levels of free testosterone decline, and levels of estrogen and insulin increase. This is partly because aging men convert much of their testosterone into estradiol, a form of estrogen. Of the remaining testosterone, much is bound to sex hormone–binding globulin, a protein in the blood, and is not biologically active. Studies have shown that men with low free testosterone have higher rates of coronary artery disease, mental depression, and dementia (Tan et al 2004).

The idea behind testosterone replacement therapy is to restore the level of free testosterone to that of a healthy 25-year-old to counteract the effects of increased estrogen. Studies have shown that fat cells, particularly abdominal fat cells, convert testosterone to estradiol (Schneider et al 1979; Kley et al 1980; Killinger et al 1987; Khaw et al 1992). The more belly fat a man accumulates, the greater the conversion of his testosterone into estradiol. As long as free testosterone is low and the ratio of estrogen to insulin is high, most aging men will store fat around their belly (Abate 2002).

Clinical studies have shown that testosterone replacement therapy can provide a variety of benefits.
In one study of 86 men aged 50 to 70, waist-to-hip ratio and blood pressure markedly decreased after 60 days of testosterone therapy (Li et al 2002).

Another testosterone-replacement study in middle-aged obese men showed improved waist-to-hip ratio along with a decrease in plasma insulin and an increase in glucose disposal, suggesting improved insulin sensitivity (Marin et al 1992).
In another trial, abdominally obese middle-aged men showed improved glucose control, decreased abdominal body fat, and improved sexual function after testosterone therapy (Boyanov et al 2003).
Given that these studies looked only at testosterone levels, one can only speculate about what the results might have looked like if excess estrogen and insulin had also been suppressed.

DHEA and Weight Loss

Testosterone and estrogen are not the only hormones implicated in weight gain. Low levels of DHEA (dehydroepiandrosterone), a steroid hormone, have also been linked to increased weight gain. Virtually everyone over age 35 experiences a significant reduction in DHEA. Studies suggest that supplementing with DHEA produces beneficial body composition changes (Villareal et al 2000; Villareal et al 2004).

For example, a 6-month trial in aging men and women with low DHEA levels demonstrated that 50 mg of DHEA per day reversed age-related changes in fat mass (Villareal et al 2000).

Another study showed that DHEA decreased abdominal obesity and improved insulin action. This randomized, double-blind, placebo-controlled trial evaluated 50 mg of DHEA per day for 6 months in 56 individuals with age-related decline in DHEA levels. The study showed that DHEA was associated with significant decreases in visceral and subcutaneous fat and improved insulin sensitivity (Villareal et al 2004).
Note: In woman DHEA can convert to testosterone, which is acceptable as long as testosterone is kept within proper range.

7-keto DHEA. A metabolite of DHEA called 7-keto DHEA has also attracted considerable attention for its value as a fat-loss supplement. Like DHEA, 7-keto DHEA levels dramatically decline with age (Marenich 1979).

In animal studies, 7-keto DHEA boosted fat-burning enzymes (Bobyleva et al 1993; Bobyleva et al 1997). Studies using 7-keto DHEA supplements produced encouraging results. For example, researchers assessed the effects of taking 100 mg of 7-keto DHEA or placebo twice daily for 60 days. Compared with placebo, the 7-keto group lost more body weight (6.3 lb vs. 2.1 lb). This study also found that supplementing with 7-keto DHEA was associated with a significantly greater percentage of body fat loss compared with the placebo group (Kalman et al 2000).

Because of the fat burning, or thermogenic effects of 7-keto DHEA, simultaneous supplementation with antioxidants is recommended to help guard against excessive free radical production. Animal studies have shown that 7-keto DHEA is not converted into testosterone or estradiol (Lardy et al 1995). Unlike caffeine or ephedra, 7-keto DHEA does not have a noradrenaline-induced central nervous system stimulating effect, nor does 7-keto increase heart rate or blood pressure.

The Insulin Trap

Recent advances in dietary science have highlighted the crucial role of insulin in weight gain. Produced in the pancreas, insulin is a critical hormone for the control of blood sugar (glucose). Its job is to transport glucose into cells, where the glucose is burned as fuel. While this process is necessary for life, abnormalities in the insulin-glucose system caused by aging, lack of exercise and poor diet can cause major health problems. In aging, cells become more resistant to the effects of insulin. As cells become increasingly insulin resistant, the body compensates by increasing the number of insulin receptors on cells and secreting more insulin in an attempt to drive more blood sugar into muscle and liver cells (Fulop 2003).

Insulin resistance is a dangerous condition. Research suggests that adipose tissue (fat) is a source of pro-inflammatory chemicals that have a role in the development of insulin resistance (Sharma AM et al 2005). Insulin resistance is associated with obesity (in particular, abdominal obesity) (Greenfield JR et al. 2004). It is also associated with aging muscle (Nair KS 2005), physical inactivity, and genetics.

This increase in insulin (called hyperinsulinemia) and decreased insulin sensitivity have a number of harmful effects, including contributing to diseases associated with being overweight (Zeman et al 2005; Garveyet al 1998).

Over time, high insulin and insulin resistance may lead to type 2 diabetes in susceptible individuals, a major risk factor for heart disease. A study sponsored by the NIH showed that over a 10-year period, hyperinsulinemia was associated with increased all-cause and cardiovascular mortality, independent of other risk factors (NIH 1985).

Controlling insulin levels as we age is essential for overall health, longevity, and weight management. An increasing number of physicians recognize the role of insulin resistance in the current obesity epidemic. The good news is that nonprescription drugs and low-cost dietary supplements that have demonstrated beneficial effects upon insulin action are already available.

http://www.lef.org/protocols/metabolic_health/obesity_01.htm