Ménière's disease

Meniere's disease / symptom:

In medical terms, it's a disease that affects the inner ear resulting in gradual hearing impairment, vertigo (dizziness), tinnitus (ringing of the ears). Severity varies, from annoyance to debilitating vertigo where the patient is unable to move.

In chiropractic terms - subluxation of the upper cervical vertebra resulting in nerve interference (nerve flow is reduced) that does not allow the body to heal itself.

Using the Gonstead Chiropractic method of specific analysis -- swelling and redness of the skin was noted on the rear hairline of the patient's neck, reduced range of motion of the upper cervical vertebra (C2 vertebra), and nervoscope indicated nerve pressure at C2/C3 spinal nerve level. Xrays revealed on the lateral view - facet imbrication, and AP view revealed PRS inferior.

Correction involved patient in the seated cervical chair, doctor's arm aiming straight up towards the ceiling to correct inferiority and reseating the C2 vertebra forward back onto C3 vertebra using a specific Gonstead seated cervical adjustment.

In the past year, 4 patients who presented with Meniere's were resolved within 2-4 weeks.




Inflammation of the upper cervical -- resulting in redness of the skin, and swelling (edema)






Meniere Patient #5 -- Lateral view shows facet imbrication (reduced space -- slight black line where circled) and C2 vertebra is inferior (tilted backwards) in relation to C3 vertebra. AP view shows C2 PRS with the dens line nearly vertical (indicates need to aim straight for ceiling). Patient received first adjustment Feb 22 2012 and scheduled for followup to see how well she is responding to the adjustment.





Full spine AP/Lat of the most severe Meniere case in my clinic. Intense debilitating vertigo like extreme sea-sickness, patient was unable to balance herself, and constant vomiting due to vertigo. Loss of hearing in both ears. Prescription medications were ineffective and netti pot had slight relief for 2 hours.




Closeup pictures. Lateral view shows facet imbrication (no space at all, completely jammed) and inferiority tilting of C2 upon C3. AP view reveals C2 PRI-inferior. Patient was adjusted C2 PR inferior twice. The 1st week reduced 80% of her symptoms, no further adjustments in week 2 or 3, her body naturally healed itself 2 weeks post-adjustment and currently asymptomatic as of this post Feb 24 2012 since Oct 2011.

Yo yo dieting increases CVD risk

We all want to lose weight... and there's nothing wrong with dieting... question is, are you losing your weight the healthy way? A recent study below shows that yo-yo dieting increases your cardiovascular disease risk.

How I lost 45 pounds and kept it off over the course of 4 years. I kept it simple and realistic.

1. Reduce sugar and sweets in your diet. So if you drink soda, replace it with water. You can lose 10 pounds right there!

2. Avoid fried foods and junk foods. All the chemicals in the foods are harmful to your body, whatever your body can't break down, it will wall off and store it away in fat as a protective defensive mechanism!

3. Eat fresh fruits and vegetables! This is key! Fresh fruits and veggies have a lot of vital enzymes and nutrients that many vitamin pills or supplements don't have. Your body needs those nutrients for optimal health. If it doesn't function right, your body can't burn the fuel (food you ate) properly and stores it away as fat!

4. Start an exercise program you enjoy doing. I admit it, I don't like to exercise but I love martial arts! Find something you love to do, whether it's basketball, swimming, gardening, doesn't matter. The key is you have to enjoy it. If you don't, you won't stick with the program.





Weight Fluctuations Among Normal-Weight Individuals Increases CVD Risk

March 5, 2010 (San Francisco, California) -- Weight cycling, where an individual's body-mass index (BMI) fluctuates during a two-year period, is associated with an increased risk of cardiovascular disease among normal-weight individuals, according to the results of a new study [1]. These weight cyclers have a risk of adverse events similar to individuals who are overweight, while overweight individuals who cycled did not experience an additional increased risk of cardiovascular events over and above the risk associated with their increased weight, report
investigators.

"We were looking at the overall weight status--how heavy the individual was between the ages of 40 and 55 years--and whether or not the weight went up and down during that period," lead investigator *Dr Molly Waring* (University of Massachusetts Medical Center, Worchester) told
*heart/wire/ *. "We found that compared with people who were normal weight, or pretty steady weight, the normal-weight individuals whose weight went up and down during the two-year period, as well as those who were overweight and obese, all had a higher risk of cardiovascular
disease and death."

The results of the study were presented here this week at *EPI|PNAM 2010*, the *Cardiovascular Disease Epidemiology and Prevention* and *Nutrition, Physical Activity, and Metabolism 2010 Conference*.

*Weight Across Time Rather Than a Point in Time*

To *heart/wire/ *, Waring said the purpose of the study was to examine patients' weight across a spectrum of years rather than a point in time to determine whether changes in weight influenced their health risk. The thinking, she said, was that a patient's weight at age 40 or 50 was less relevant than weight over the course of a lifetime.

Using data from the *Framingham Heart Study*, the researchers quantified the effect of overall weight status and weight cycling in 1429 participants aged 40 to 55 years old. Weight status and weight cycling was categorized using component scoring that allowed researchers to capture the weight patterns across middle age. In this study, weight cycling was defined as a change of one BMI unit within the two-year period. That works out to be about five pounds for an individual who is five feet tall and seven pounds for six-foot tall male, said Waring.

Results showed that compared with an overall normal-weight trajectory without weight cycling, normal-weight individuals whose weight went up and down over the study period had a 50% greater risk of cardiovascular disease events and a 40% greater risk of cardiovascular mortality. These normal-weight cyclers were also at a significantly increased risk of cerebrovascular accidents and coronary heart disease events when compared with normal-weight individuals whose weight did not fluctuate.

*Risks of Cardiovascular Disease and Cardiovascular Mortality*

Events


Adjusted hazard ratio (95% CI)

*Cardiovascular disease events*



*Normal weight, no cycling*



Referent

*Normal weight, cycling*



1.5 (1.2-2.0)

*Overweight, no cycling*



1.7 (1.3-2.2)

*Overweight, cycling*



1.8 (1.4-2.2)

*Obese*



2.7 (2.0-3.5)

*Cardiovascular mortality *



*Normal weight, no cycling*



Referent

*Normal weight, cycling*



1.4 (1.0-2.0)

*Overweight, no cycling*



1.3 (0.9-2.0)

*Overweight, cycling*



1.6 (1.1-2.2)

*Obese*



1.8 (1.1-2.9)

Comparatively, overweight individuals who maintained a constant weight and those whose weight cycled during middle age had similar risks of cardiovascular, cerebrovascular, and coronary heart disease events. In addition, they had similar risks of cardiovascular and overall mortality.

"Among people who are overweight, those whose weight varied within the two-year period were not at any higher risk of cardiovascular disease and death than those overweight individuals whose weight remained steady," said Waring. "I think that's a positive finding from the study,
because we know how difficult it is for patients to lose weight and to keep it off. It's encouraging in that if they are trying to lose weight but gain it back because they're not able to maintain the lifestyle changes, it's not putting them at greater risk. The message is to keep trying."

For normal-weight patients, this study emphasized the importance of keeping the weight off, because even periods of normal weight won't protect against cardiovascular disease events if the patients' weight fluctuates up and down, she said.

References

1. Waring ME, Eaton CB, Lapane KL, et al. Weight cycling and overall
weight status during middle age and incident cardiovascular
disease events and all-cause and cardiovascular mortality.
EPI|PNAM 2010; March 3, 2010; San Francisco, CA. Abstract P138.

Dieting tips...

Here's one simple way to lose weight...

Chew and eat your food SLOWLY

A recent study shows that "wolfing" your food can make you gain weight. By eating quickly, like what most New Yorkers do, it doesn't properly signal your body that nutrition is coming down it's way. In essence, that "I'm Full" signal gets delayed, which causes you to overeat more calories than your body needs.

Wolfing down food also puts more strain on your digestive tract. Chewing food helps to physically break down the food so the acid and enzymes in the stomach and small intestines don't have to work nearly as hard. In addition, we release some digestive enzymes in our mouth during chewing. So, would it come to anyone surprise why we would get indigestion or belly aches more so when we quickly overeat?

If you have that issue of eating quickly but can't slow down, how about choosing a different food to eat. Meals that are processed or fast foods may be quicker to eat but they pack on a lot of calories. Eating fresh raw fruits forces you to slow down and physically chew the food. Also, considering it takes about 4-5 bites to eat one hamburger that's loaded with 300-500 calories, that same 4-5 bites into a fresh Apple has 120-180 calories. Not only is it less calories, it also has more enzymes and nutrients than a fatty hamburger.

So, grab that fruit!


Dr. Suh, DC
www.gonsteadny.com

Use of Low-Dose Aspirin in Primary Prevention of Cardiovascular Events Not Recommended

August 30, 2009 (Barcelona, Spain) — The use of low-dose aspirin in the primary prevention of cardiovascular events in healthy individuals with asymptomatic atherosclerosis is currently not warranted, according to the lead researcher of a large "real-world" study presented today at the European Society of Cardiology (ESC) 2009 Congress.

In the randomized trial of 3350 subjects deemed at high risk for cardiovascular and cerebrovascular events because of a low ankle-brachial index (ABI) (<0.95), aspirin had absolutely no effect on reducing events compared with placebo, Dr Gerry Fowkes (University of Edinburgh, Scotland) reported on behalf of the Aspirin for Asymptomatic Atherosclerosis (AAA) trialists.

However, aspirin did increase the risk of major hemorrhage.

The bleeding effect "is a real obstacle," Fowkes told heartwire . "I don't think the evidence is convincing enough as yet that aspirin should be used routinely in the general population."

The results of the trial are in conflict with findings from a meta-analysis from the Antithrombotic Trialists' (ATT) collaboration, which was published earlier this year in the Lancet [1], discussant Dr Carlo Patrono (Catholic University School of Medicine, Rome, Italy) told ESC attendees. He questioned how the results of AAA could be interpreted in light of the 12% relative risk reduction in serious cardiovascular events, largely driven by a reduction in nonfatal MI, that was seen in the ATT trial.

AAA Done Where the Need for Prevention Is Great

The AAA was a pragmatic trial, Fowkes explained, conducted in a deprived population in central Scotland, where rates of coronary heart disease and related mortality are high. "We wanted to get at where the problem actually existed in the population," he said.

Between 1998 and 2001, the AAA trialists invited men and women 50 to 75 years of age to undergo screening for asymptomatic atherosclerosis by measuring their ABI. A low ABI in otherwise-healthy individuals has been shown to be related to an increased risk of future cardiovascular events. Because it is simple and noninvasive, the ABI has the potential to be used as a screening test to detect high-risk individuals, Fowkes explained.

Of the more than 166 000 invitations that were sent out, the trialists ended up screening 28 980 individuals. Of this number, 3350 had a low ABI and were thus eligible to be entered into the trial.

They were randomly allocated to 100-mg enteric coated aspirin daily or to placebo and followed for a mean of 8.2 years. The primary end point of the trial was the composite of an initial fatal or nonfatal coronary event, stroke, or revascularization. Secondary end points were all vascular events, which included a composite of initial fatal or nonfatal coronary event, stroke, or revascularization, angina, intermittent claudication, transient ischemic attack, and all-cause mortality.

Patients in both groups were matched for age (mean age 62 years), gender (roughly 30% were men), and comorbidities. One-third of the study population consisted of smokers.

Aspirin had no effect in terms of reducing cardiovascular and cerebrovascular events. In all, there were 357 events, 181 (10.8%) in the aspirin group and 176 (10.5%) in the placebo group (hazard ratio 1.03, 95% CI 0.84–1.27).

Primary End-Point Results for Aspirin vs Placebo
End point Aspirin (n=1675), n (%) Placebo (n=1675), n (%)
Fatal coronary event 28 (1.7) 18 (1.1)
Fatal stroke 7 (0.4) 12 (0.7)
Nonfatal coronary event 62 (3.7) 68 (4.1)
Nonfatal stroke 37 (2.2) 38 (2.3)
Coronary revascularization 24 (1.4) 20 (1.2)
Peripheral revascularization 23 (1.4) 20 (1.2)

Interestingly, cancer mortality was higher in the placebo group than in the aspirin group, Fowkes noted.

Adverse events, including major hemorrhage, were greater in the aspirin group (HR 1.71, 95% CI 0.99–2.97).

Adverse Events With Aspirin vs Placebo
Adverse event Aspirin (n=1675), n (%) Placebo (n=1675), n (%)
Major hemorrhage 34 (2.0) 20 (1.2)
Gastrointestinal ulcer 14 (0.8) 8 (0.5)

Fowkes pointed out that 40% of patients were noncompliant and did not take their aspirin as prescribed over the duration of the trial. Such a low compliance rate could have affected the results. "The 60% compliance rate is the typical level of compliance that you will find in the primary-prevention setting, and obviously there are many reasons that people stop taking aspirin. So whether aspirin is beneficial in clinical practice among patients who have a low ankle-brachial index and who are fully compliant with aspirin is unknown, and so our results cannot be extrapolated to that situation," he said.

heartwire asked Fowkes what he thinks may work for primary prevention in people with asymptomatic atherosclerosis, now that aspirin appears to be ineffective. "We don't have any strong evidence about what would work, but I think that given that these are high-risk individuals, it is probably reasonable to give them a statin. I think it would prove to be cost-effective to give a statin," he said. "Obviously, there is the possibility of giving a stronger antiplatelet such as clopidogrel or some of these new drugs that are being developed, but one would have to trial those properly."

AAA Underpowered

Patrono said the AAA study may have been underpowered and suggested that was one reason for its negative findings. "The sample size would have to be about four times larger to achieve the power to show a 12% relative risk reduction," he said.

Other reasons: "The presence of peripheral arterial disease, whether symptomatic or asymptomatic, may render platelet activation more critically dependent on ATP than thromboxane release, and there is some experimental as well as clinical evidence supporting this possibility."

An accelerated platelet turnover associated with peripheral arterial disease--at least in some patients--may also be a cause for the discrepancy, Patrono said.

To try to dissect out potential explanations, Fowkes and Dr Colin Baigent (Oxford University, UK), lead author of the ATT trial, have agreed to see how the AAA study would fit into the ATT meta-analysis. When available, the results will be posted by the Clinical Trial Service Unit, Patrono said.

Fowkes told heartwire that there is no reason to think that the relative reduction in cardiovascular events created by aspirin should be different in the primary or secondary setting. It's just that the benefits in the secondary setting far outweigh the risks. "The absolute reduction is much higher in secondary prevention than in primary prevention, but the level of bleeding is the same. So in secondary prevention, you've got a big reduction in events and a small amount of bleeding. In primary prevention, you have a smaller amount of reduction of events, and the same amount of bleeding. These two have got to be counterbalanced in the primary-prevention situation, and that is where the concern is at the moment."

Packaged Meat

Be careful of what you buy. Even more reason to buy Organic meat.

Flaxseed Reduces Blood Lipids

Instead of relying on statin medications which have side-effects, including depriving your heart of Co-Enzyme Q10 for proper function, consider using Flax seed or fish oil which provides Omega 3 essential fatty acids to reduce your cholesterol and LDL levels!

Dr. Ryan Suh, DC
www.gonsteadny.com




July 29, 2009 — Whole flaxseed and flaxseed lignans significantly reduce circulating total cholesterol and low-density lipoprotein (LDL) cholesterol levels, showing their greatest effect in postmenopausal women and individuals with high initial cholesterol concentrations, according to the results of a meta-analysis published in the August 2009 issue of the American Journal of Clinical Nutrition.

"Owing to the promising results in preclinical models, many clinical trials have been performed to determine the outcomes of flaxseed intervention (whole flaxseed, flaxseed oil, or lignans) on various cardiometabolic risk factors, particularly blood lipids," write An Pan, MSc, from the Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Chinese Academy of Sciences, Shanghai, China, and colleagues. "However, the findings from most of the previous clinical trials were inconsistent, and the discrepancies could be attributed to small sample size, insufficient study duration, variation in study designs, and diversity of the test product."

Total, LDL Cholesterol Levels Reduced

The aim of this study was to evaluate whether administration of flaxseed or its derivatives could improve total, LDL, and high-density lipoprotein (HDL) cholesterol levels and triglyceride levels by making use of the increased statistical power afforded by a meta-analysis.

The researchers searched all randomized controlled trials of flaxseed or its derivatives on lipid profiles in adults, which were published in English from January 1990 to October 2008. They also attempted to contact authors of unpublished data. Study quality was assessed with use of the Jadad score; 16 studies were classified as high quality (Jadad score of 4 or 5), and 12 studies were classified as low quality (Jadad score of 2 or 3).

The 28 trials used in the meta-analysis comprised a total of 1381 study subjects. Five were conducted exclusively in postmenopausal women, 1 was done in premenopausal women, 10 trials were conducted in men, 10 trials were conducted in both sexes, 1 trial did not indicate the sex composition of the study sample, and 1 trial reported results separately by sex.

The median duration of the trials was 8.5 weeks, (range, 2 - 52 weeks). Flaxseed in whole, ground, or defatted form was tested in 10 of the 28 trials in doses that ranged from 20 to 50 g (2 - 5 tablespoons), and flaxseed oil was tested in 13 of the trials.

A significant reduction in total cholesterol levels was found in studies using whole flaxseed, with a net change of –0.19 mmol/L (95% confidence interval [CI], –0.29 to –0.09 mmol/L) and also in studies using lignan supplements, where the net change was –0.28 mmol/L (95% CI, –0.55 to –0.01 mmol/L). Similarly, a significant reduction in LDL cholesterol levels was found with whole flaxseed (net change, –0.16 mmol/L; 95% CI, –0.25 to –0.06 mmol/L) and lignan supplements (–0.16 mmol/L; 95% CI, –0.31 to –0.01 mmol/L). However, there were no significant changes in total and LDL cholesterol levels with the intervention of flaxseed oil, the study authors report.

Women vs men had greater reductions in total cholesterol levels with flaxseed. The mean reduction for women was –0.24 mmol/L (95% CI, –0.36 to 0.12 mmol/L), and for men, the mean reduction was –0.09 mmol/L (95% CI, –0.05 to 0.23 mmol/L). The same was found with reductions in LDL cholesterol levels: for women, the mean reduction was –0.17 mmol/L (95% CI, –0.28 to –0.06 mmol/L), and for men, the mean reduction was –0.07 mmol/L (95% CI, –0.04 to 0.18 mmol/L).

The authors also report that total and LDL cholesterol levels were reduced to a greater degree in the high-quality studies (net change, –0.13 mmol/L; 95% CI, –0.24 to –0.02 mmol/L) vs the low-quality studies (net change, –0.08 mmol/L; 95% CI, 0.16 to –0.01 mmol/L). No significant changes were detected in the low-quality studies, they add.

When the studies were stratified according to initial lipid status, significant reductions in total cholesterol levels were found in the studies including subjects with high initial concentrations, defined as 5.7 mmol/L for total cholesterol and 3.4 mmol/L for LDL cholesterol. For these individuals, the mean change in total cholesterol level was –0.17 mmol/L (95% CI, –0.32 to –0.03 mmol/L), and the mean change in LDL cholesterol level was –0.13 mmol/L (95% CI, – 0.23 to –0.02 mmol/L). In comparison, the mean change in total cholesterol levels for subjects with lower initial concentrations was 0.03 mmol/L (95% CI, –0.11 to 0.17 mmol/L), and the mean change in LDL cholesterol levels was 0.00 mmol/L (95% CI, –0.12 to 0.12 mmol/L).

There were no significant changes in HDL cholesterol or triglyceride levels.

Interpret Findings With Caution

The authors point out that the limitations of their study include the heterogeneity of the studies in the meta-analysis, and a lack of information on the quality, quantity, and bioavailability of the flaxseed that was used. Therefore, they write, their findings must be interpreted with caution.

The results of this meta-analysis indicate that flaxseed consumption may be a useful dietary approach for the prevention of hypercholesterolemia, especially in some patient subgroups, the authors conclude. They add that further studies should be done to investigate the effectiveness of flaxseed supplementation on cardiometabolic risk factors other than blood lipids and, ultimately, on cardiovascular disease–related morbidity and mortality.

Dr. Pan has disclosed no relevant financial relationships.

Am J Clin Nutr. 2009;90:288-297.Abstract