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Thirdhand smoke consists of residual tobacco smoke pollutants that remain in the house

Thirdhand smoke consists of residual tobacco smoke pollutants that 1) remain on surfaces and in dust after tobacco has been smoked, 2) are re-emitted back into the gas phase, or 3) react with oxida…

Source: Thirdhand smoke consists of residual tobacco smoke pollutants that remain in the house

Thirdhand smoke consists of residual tobacco smoke pollutants that remain in the house

Thirdhand smoke consists of residual tobacco smoke pollutants that 1) remain on surfaces and in dust after tobacco has been smoked, 2) are re-emitted back into the gas phase, or 3) react with oxidants and other compounds in the environment to yield secondary
figure ehp-119-a70f2

Michael Siegel of Boston University School of Public Health believes one potentially meaningful question is whether significant exposure to toxic THS constituents could occur as a result of smoke absorbed onto a smoker’s clothing. “This
figure ehp-119-a70f3

Georg Matt of San Diego State University points out that in the absence of any hard evidence of actual long-term health effects of THS, many nonsmokers—and former smokers—have already been sensitized to the phenomenon. “The most

You may never have heard of thirdhand smoke, or THS, but chances are you’ve smelled it. THS is, in the words of The New York Times, “the invisible yet toxic brew of gases and particles clinging to smokers’ hair and clothing, not to mention cushions and carpeting, that lingers long after secondhand smoke [SHS] has cleared from a room.”1 Recent research exploring potential dangers of THS has received a flurry of coverage in the international media2,3,4 and the scientific press.5,6,7 And in the United States, court cases are beginning to appear in which plaintiffs are citing these alleged dangers,8,9 despite a lack of human health studies on the long-term health effects of THS exposure.

So how dangerous might THS really be? The answer, still to be pronounced, will depend on many factors.

THS was a topic of interest long before it received its present name. The seed of the idea that cigarette smoke toxicants might linger on room and car surfaces long after the smoke itself was gone was planted in 1953, when it was reported that smoke condensate painted onto mice caused cancer.10

In 1991 the house dust of smokers’ homes was first found to be contaminated with nicotine.11 Later, in 2004, nicotine was quantified in the dust of nonsmokers’ homes and homes in which mothers smoked in the house over the preceding 3 months.12 In homes with the highest SHS exposure, in which the mothers smoked in areas where their children were present, nicotine in dust averaged 64.0 μg/m2 in living rooms and 15.8 μg/m2 in infants’ bedrooms. Surfaces in living rooms and infants’ bedrooms averaged nicotine coatings of 73.05 μg/m2 and 56.26 μg/m2, respectively. The same study showed the dust and surfaces of homes in which smokers had tried to limit their children’s exposure (for instance, by sometimes smoking outdoors) were also contaminated, although to a lesser degree. However, no nicotine was found in the dust or on the surfaces of homes never exposed to tobacco smoke.12

In 2008 similar findings were reported for cars.13 Nicotine was detected in significantly greater quantities in the dust (mean 19.51 μg/g) and on the dashboards (mean 8.61 μg/m2) of 78 vehicles belonging to people who smoked in their vehicles than in the dust (mean 3.37 μg/g) and on the dashboards (mean 0.06 μg/m2) of 20 vehicles of nonsmokers. Eight smokers had imposed a smoking ban in their vehicles for at least 12 months. Their vehicles nevertheless were contaminated with nicotine (mean 11.61 μg/g in dust and 5.09 μg/m2 on the dashboard). The authors point out, however, that the cars may have been contaminated by smoke that entered the car from outside and that smoking bans may not have been complied with 100% of the time.

A 2010 study showed THS also remains after smokers move out of their homes, even after being vacant for two months and being prepared for new residents, sometimes with new carpeting and paint.14 Meanwhile, other lines of research have confirmed some smoke compounds adsorb onto surfaces and then desorb back into the air over time, providing a source of tobacco toxicants that lingers long after people finish smoking

Side effects of Statins – avoid sugar and trans-fat to lower cholesterol

Statin drugs impair important biochemical functions in your body and deplete the supply of the coenzyme CoQ10, leading to fatigue, heart failure, muscle weakness and soreness. From  : The statins (…

Source: Side effects of Statins – avoid sugar and trans-fat to lower cholesterol

Side effects of Statins – avoid sugar and trans-fat to lower cholesterol

Statin drugs impair important biochemical functions in your body and deplete the supply of the coenzyme CoQ10, leading to fatigue, heart failure, muscle weakness and soreness. From  : The statins (…

Source: Side effects of Statins – avoid sugar and trans-fat to lower cholesterol

Side effects of Statins – avoid sugar and trans-fat to lower cholesterol

Statin drugs impair important biochemical functions in your body and deplete the supply of the coenzyme CoQ10, leading to fatigue, heart failure, muscle weakness and soreness.

From http://mpkb.org/home/othertreatments/statins :

The statins (or HMG-CoA reductase inhibitors) along with other drugs, such as cholestyramine (Questran), comprise the class of hypolipidemic drugs. Hypolipidemic drugs are prescribed – sometimes aggressively so – to lower cholesterol levels in people with or at risk of cardiovascular disease and certain inflammatory diseases such as sarcoidosis. Statins are prescribed even though their full mechanisms of action remain unclear. One strong possibility is that statins exert their effects via the body’s nuclear receptors, which are intricately connected to innate immune function.

The statins have a range of documented negative effects, some of which may be immunopathological. Because statins may interfere with the Marshall Protocol, these drugs are contraindicated.

Statins interfere with the actions of Olmesartan, as they are a very similar molecule, and compete with Olmesartan for many of Olmesartan’s molecular binding sites. The actions of statins on the Nuclear Receptors are therefore competitive with Olmesartan, as they reduce or negate Olmesartan’s therapeutic activities.

As the 2008 ENHANCE trial illustrates, while high cholesterol is correlated with increased incidence of diseases, lowering cholesterol does not appear to improve human health.1) Indeed, there is some evidence this type of intervention does the opposite.

Statins

The following is a list of common cholesterol-lowering drugs known as statins:

  • atorvastatin (Lipitor)
  • cholestipol (Cholestid)
  • colesevalam HCL (Welchol)
  • fluvastatin (Lescol)
  • lovastatin (Mevacor)
  • ezetimibe (Zetia)
  • ezetimibe and simvastatin (Vytorin)
  • fenofibrate (Tricor)
  • pravastatin (Pravachol)
  • rosuvastatin (Crestor)
  • simvastatin (Zocor)

Other cholesterol drugs

The following is a list of common non-statin cholesterol-lowering drugs:

  • cholestyramine (Questran) – Part of another treatment protocol, cholestyramine is touted to relieve symptoms supposedly caused by the release of toxins as the Lyme spirochete is killed. However, cholestyramine is known to interfere with the action of tetracycline, an antibiotic in the same class – the tetracycline family of antibiotics – used by many of the MP antibiotics.
  • gemfibrozil (Lopid, Gemcor)
  • Omacor
  • pantethine
  • red yeast rice (monascus purpureus)

Ravnskov compares two separate trials of a single statin, simvastatin: a 2002 trial (nicknamed HPS)6) and a 1994 study (nicknamed 4S)7). The 4S research team reported a three times greater risk of coronary death in the HPS trial, even though patients’ total cholesterol in the 4S trial was decreased to a much lower extent.8)

A seminal study called the ENHANCE trial was published in 2008. The trial tested the effects of a new cholesterol-lowering medication called Zetia (which, as opposed to the statins, works by decreasing cholesterol absorption in the intestine) on patients with cardiovascular disease. It found that Vytorin, a combination pill containing both Zetia and the statin Zocor (simvastatin), proved better than the statin alone at reducing levels of cholesterol. However, ENHANCE collaborators reported that Vytorin resulted in growth of plaque.9)

All together, this evidence suggests statins’ ability to (slightly) improve health outcomes is independent of their ability to lower cholesterol.10)

Statins may alter nuclear receptor activity

Statins are now known to alter nuclear receptor activity, and it may be the effects which result from these mechanisms that account for in health outcomes of patients taking the drugs. (Note: Zetia, which is not a statin, does not seem to have this property.)

Statins have been demonstrated to increase CYP3A expression in vitro, most likely because they are ligands to nuclear receptors (pregnane X receptor and constitutive androsterone receptor) that form heterodimers with retinoid X receptors and bind to responsive elements in the CYP3A4 and CYP3A5 promoter regions.

M.A. Willrich 11)

Because each of the statin has such different affinities for the receptors they bind, each works in different ways and influences the transcription of different genes. Some may activate the nuclear receptors while others might slow their activity. Indeed, this may explain the variability in side effects between one statin and the next.

Simvastatin, rosuvastatin and atorvastatin work in vastly different ways. They may each benefit people under different conditions but we have no way of knowing exactly how at this point.

Trevor Marshall, PhD

Immunopathological effects of statins?

According to the reports from the statin trials, all of which have been sponsored by the drug companies, side effects are mild and rare, but underreporting is prevalent. According to drug companies, muscular symptoms occur in less than one percent of patients taking statins, however researchers independent of drug companies have found the frequency to be 64%12) and 75%.13) In the IDEAL trial, almost 90% of participants in both groups had side effects, and in almost half of them they were recorded as serious.14) The following adverse effects for statins have been noted in the medical literature:

  • increased incidence of lupus and pneumonia15) – Note the similarity between “statin-induced lupus” and “minocycline-induced lupus.”16)
  • dyspnea (pain while breathing) – Those with pulmonary involvement such as sarcoidosis patients sometimes confuse their disease symptoms with the side effects of statins.
  • muscle pain17) 18)
  • renal dysfunction — Statins appear to be able to cause proteinuria through tubular inhibition of active transport of small molecular weight proteins.19) 20)
  • tendon complications21)
  • cognitive dysfunction – A 2008 survey of statin patients found that 75% experienced cognitive dysfunction determined to be probably or definitely related to statin therapy. Of 143 patients who reported stopping statin therapy, 90% reported improvement in cognitive problems, sometimes within days of statin discontinuation with a median time to recovery of 2.5 weeks. In some patients, a diagnosis of dementia or Alzheimer’s disease reportedly was reversed. Severity of cognitive problems were clearly related to statin potency.22)
  • fatigue – Almost half of participants in a 2012 study reported a significant increase in fatigue while taking statins.23)

As discussed in the previous section, it may be that their effect on nuclear receptors explain how some statins increase patients’ disease symptoms. Indeed, a 2009 Pathology paper described antimicrobial activity of atorvastatin and rosuvastatin.24) Some of the observed side effects of statins may be immunopathological in nature. One study reports both bactericidal and inflammatory response changes in macrophage activity from simvastatin. 25) It is possible that statins have similar immune-activating properties to the main drug for the Marshall Protocol, olmesartan, which causes an increase in disease symptoms following bacterial death.

However, olmesartan has several advantages over the statins including a superior safety profile,26) demonstrated ability to decrease plaque formation,27) and renoprotective properties.28)

In any case, researchers tend not to study or discuss what may be statins’ primary mechanism of action: its effect on immune function. Nor, is their an earnest exploration of how modulating immune activity against chronic microbes29) affects the course of human disease.

Contraindications of statins

In particular, the following drugs seem to make the statins more likely to cause problems:

Statins may alter nuclear receptor activity

Statins are now known to alter nuclear receptor activity, and it may be the effects which result from these mechanisms that account for in health outcomes of patients taking the drugs. (Note: Zetia, which is not a statin, does not seem to have this property.)

Statins have been demonstrated to increase CYP3A expression in vitro, most likely because they are ligands to nuclear receptors (pregnane X receptor and constitutive androsterone receptor) that form heterodimers with retinoid X receptors and bind to responsive elements in the CYP3A4 and CYP3A5 promoter regions.

M.A. Willrich 11)

From http://www.goodrx.com/blog/non-statin-cholesterol-medication-that-works-introducing-juxtapid/:

Aside from Zetia there haven’t been any good non-statin options for lowering LDL Cholesterol. Statin drugs like Lipitor (atorvastatin), Zocor (simvastatin) and Crestor work well to lower the “bad” cholesterol, the LDL, and have remained first line therapy for many years. Finally, there may be something new to get excited about. But, it does have some “issues.”

Juxtapid is a new medication approved for lowering cholesterol. For now it is approved for use only in patients with familial hypercholesterolemia already on statin mediations. Those are patients with extreme elevations in LDL cholesterol and high risk of early heart disease. It is unknown whether Juxtapid will eventually receive approval for the treatment of high cholesterol in all adults.

Juxtapid is not a statin, and is the first in a new class of medications called microsomal triglyceride transfer protein (MTP) inhibitors. Expect more from that class.

How do we know it works? When added to statin therapy in patients with familial hypercholesterolemia,Juxtapid significantly reduced LDL by 40 – 50%, which is huge.

Juxtapid has issues, however, that will prevent it from being a game changer for cholesterol. Its side effect profile stinks. Twenty eight percent of patients studied had diarrhea, nausea, vomiting or abdominal pain. Ugh. Juxtapid also caused a bump in liver function blood tests in 34% of treated folks. Based on these results, liver tests have to be obtained before and during treatment. This is the same hassle faced with the statin drugs (Lipitor, Zocor, Crestor, etc.). It works well, but at a cost.

Natural way to lower cholesterol using colorful whole foods and exercise

Limit your intake of foods full of saturated fats, trans fats, and dietary cholesterol. Add fiber and fish (Omega 3) in your diet. Always select colorful plants as your whole foods diet. Stay away from allergens, stress and infection. Strengthen blood vessels with Vit C, A and E. Avoid sugar and grains

Both polyunsaturated and monounsaturated fatty acids help lower LDL. Most plant-derived oils, including canola, safflower, sunflower, olive, grapeseed, and peanut oils, contain both. Fatty fish (such as salmon, tuna, trout, herring, and mackerel), seeds, nuts, avocados and soybeans are also great sources.

Foods with a lot of saturated fat include butter, fatty flesh like red meat, full-fat and low-fat dairy products, palm oil, and coconut oil. If you see partially hydrogenated fat in the Ingredient List of a food label, that food has trans fats. Top sources of dietary cholesterol include egg yolks, organ meats, and shellfish.

One type of fat – omega-3 fatty acids – has been shown to protect against heart disease. Good sources are cold-water fish like salmon, mackerel, halibut, trout, herring, and sardines.

To help you translate the above guidelines into daily food planning, here are key guidelines:

Select nonfat dairy foods only, 2 servings daily.

Limit your intake of meat, poultry, and fish to no more than 3.5 to 4 ounces per day. From the choices below, which are listed from best to poor, try to select almost always from the top.

Best Choice: Omega-3-rich fish, such as salmon, sardines, herring, mackerel, and trout. Choose at least 2 times weekly. If you’re using canned fish, such as canned sardines, select very-low-sodium or no-salt-added varieties.

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Federal Gift and Estate Law in 2016 and Beyond

By Mary Randolf

For the foreseeable future, the federal estate tax will continue to affect only the richest families in America. Under legislation passed by Congress on New Year’s Day 2013, the estate tax exemption was made permanent at the $5 million 2012 rate, but adjusted for inflation each year. Of course, calling the tax law “permanent” doesn’t mean Congress couldn’t change it again, but little energy is being directed at estate tax legislation now.

Exemption Amounts

In 2016, every person may leave or give away up to $5.45 million without owing any estate tax. As a practical matter, that means that under the new rules about 99.5% of all estates will NOT owe any federal gift/estate tax. The exemption amount is indexed for inflation each year. Unlike legislation enacted in the last several years, there is no sunset provision for these amounts; indexed for inflation, they will stay in force until Congress changes them again.

‘Portability’ for Spouses

One popular feature of the current estate tax law is that spouses can combine their estate tax exemptions, effectively letting married couples give away or leave almost $11 million without owing tax. The new law makes this feature, called “portability” by tax experts, permanent.

Here’s how it works: If the first spouse to die doesn’t use up his or her individual gift/estate tax exemption, the surviving spouse can use what’s left. That gives the couple a total exemption of twice the individual exemption amount. They can share that total exemption amount in the way that provides the greatest tax benefit. For example, if each member of a couple has $4 million in assets, and the first one to die leaves everything to the other, no estate tax is owed because property left to a spouse is tax-free. When the survivor dies and leaves $8 million ($4 million plus the $4 million inherited from the other spouse) to their children, no estate tax will be due, even though the estate is over the exemption amount, because the estate can use some of the first spouse’s unused exemption.

To take advantage of the portability rule, an estate tax return must be filed when the first spouse dies–even if no tax will be due. As commentators have pointed out, this means the IRS must process returns that don’t provide any tax revenue, and taxpayers must pay experts to prepare these very complicated tax returns.

Gift and Estate Tax Rates

On very large estates subject to the tax, the gift/estate rate is now 40%, lower than the rates in almost every year since the 1930s.

This rate also applies to the generation-skipping transfer tax. That is a federal tax that is imposed on large transfers that skip a generation (for example, a gift from a grandparent to a grandchild) in an attempt to avoid estate tax.

Learn more about Estate Tax on Nolo.com.