Keeping our brain healthy from birth to 100

Keeping our brain healthy from birth to 100

December 1,2018 at JCC in Palo Alto California

Speakers and event sponsors are welcome. All older adults are invited.

2-5pm, Bldg D room

Tips for healthy brain

Other speakers:
Connie Dello Buono – Health blogger and Motherhealth caregivers founder at www.clubalthea.com

Contact motherhealth@gmail.com for details or text 408-854-1883

Oshman Family Jewish Community Center, Room in Building D.

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Flyer

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Growth hormone (GH) , asthma meds and muscle quality

Growth hormone (GH) and muscle quality

GH production drops by 60% at age 60. A senior who had been taking asthma meds for a long time experienced severe neck and shoulder bone fracture from a fall.  Know that some meds can impair muscle quality.

The following factors influence GH secretion spike by the pituitary gland in the brain:

Factors Increasing GH Secretion Factors Decreasing GH Secretion
Physiological: Physiological:
Sleep Hyperglycemia
Fasting Elevated Blood Free Fatty Acids
Exercise Obesity
High Amino Acids
in the Blood
Hyper or Hypothyroidism
Low Blood Sugar  
Pharmacologic: Pharmacologic:
Any hypoglycemic agent GH itself
Estrogens Somatostatin
Alpha-agonists Alpha antagonists (yohimbine)
Beta antagonists Beta agonists (ephedrine, clenbuterol)
Serotonin Serotonin antagonists
Dopamine Dopamine antagonists
GABA  

Source: Basic and Clinical Endocrinology, 5th Edition

Muscle regeneration

Muscle growth and capacity to regenerate upon injury are faster for skeletal muscle but poor for cardiac muscle especially for young ones.

A greater capacity for regeneration of cardiac muscle is seen in fish. Fish oil, folate, Vitamin Bs, Coenzyme Q10 and omega 3 dietary supplements are important for our heart muscles.

Skeletal muscle has an excellent capacity for regeneration.  Inflammation and innervation makes regeneration suboptimal for seniors.

As we age, our cardiac muscles are easily affected even from those who have regular exercise and eat healthy.

Muscle regeneration is the process by which damaged skeletal, smooth or cardiac muscle undergoes biological repair and formation of new muscle in response to death of muscle cells.

Key Concepts:

  • Necrosis is required for muscle regeneration.
  • Inflammation is essential to remove necrotic tissue and initiate myogenesis.
  • New blood vessel formation is required after major injury of muscles.
  • Reinnervation is essential for functional recovery of skeletal muscle.

Adult skeletal muscle is a postmitotic tissue, accomplished by resident stem cells, satellite glial cells (SGCs). Current theories suggest that SGCs are important in controlling the microenvironment of the sympathetic ganglia.

SGCs role as a regulator of neuronal microenvironment is further characterized by its electrical properties which are very similar to those of astrocytes. Astrocytes have a well-studied and defined role in controlling the microenvironment within the brain.

First trimester health of fetus and leukemia, Leukemia inhibitory factor

This wiki info on Leukemia inhibitory factor details when this LIF cytokine is expressed:  LIF is normally expressed in the trophectoderm of the developing embryo.

My mother’s friend is an alcoholic and birthed a daughter who had leukemia later at 20 yrs old and a son with behavioral issues. She has survived leukemia. Her son is working but always fight with her.

I urged all new mothers to lead a healthy life before and during pregnancy since all medications, alcohol and the environment affects the growing embryo. And behavioural issues also happens later in the children’s life including cancer/leukemia.

Connie


From Wiki

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation. When LIF levels drop, the cells differentiate.

Function

LIF derives its name from its ability to induce the terminal differentiation of myeloid leukemic cells, thus preventing their continued growth. Other properties attributed to the cytokine include: the growth promotion and cell differentiation of different types of target cells, influence on bone metabolism, cachexia, neural development, embryogenesis and inflammation. p53 regulated LIF has been shown to facilitate implantation in the mouse model and possibly in humans.[3] It has been suggested that recombinant human LIF might help to improve the implantation rate in women with unexplained infertility.[4]

Binding/activation

LIF binds to the specific LIF receptor (LIFR-α) which forms a heterodimer with a specific subunit common to all members of that family of receptors, the GP130 signal transducing subunit. This leads to activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen activated protein kinase) cascades.[5]

Expression

LIF is normally expressed in the trophectoderm of the developing embryo, with its receptor LIFR expressed throughout the inner cell mass. As embryonic stem cells are derived from the inner cell mass at the blastocyst stage, removing them from the inner cell mass also removes their source of LIF.

Pregnancy

Leukemia inhibitory factor is a cytokine expressed in the uterus during the secretory phase of the menstrual cycle, as well as expressed during a normal pregnancy.[6] Specifically, LIF is expressed in uterine endometrial glands and is under maternal control.[7]When the fertilized zygote has reached the blastocyst stage, the stromal cells surrounding the blastocyst produce leukemia inhibitory factor, which needed for the blastocyst to implant into the uterine endometrium.[6]

During pregnancy leukemia inhibitory growth factor is involved in decidualization of the maternal endometrium and implantation of the blastocyst to the endometrium.[6] LIF levels are highest on the fourth day of pregnancy indicating its involvement in implantation.[7]Implantation is critical in pregnancy in order to establish the placenta and maternal-fetal interface. Fetal endothelial cells also express the receptor for leukemia inhibitory factor, indicating it may be involved in placental angiogenesis.[8] There is also evidence leukemia inhibitory factor is involved in the survival and proliferation of primordial germ cells, which are the cellular origins of spermatozoa and oocytes.[9]

Decreased secretion of leukemia inhibitory factor is associated with poor or no implantation and, thus, pregnancy loss. Women with decreased production of LIF and other cytokines are fertile and able to become pregnant, but there is an increased risk for unexplained, recurrent miscarriages.[7][10]

Use in stem cell culture

Removal of LIF pushes stem cells toward differentiation, but they retain their proliferative potential or pluripotency. Therefore LIF is used in mouse embryonic stem cell culture. It is necessary to maintain the stem cells in an undifferentiated state, however genetic manipulation of embryonic stem cells allows for LIF independent growth, notably overexpression of the gene Nanog.

LIF is typically added to stem cell culture medium to reduce spontaneous differentiation.

Treatment gaps in rheumatoid arthritis

By Rita Baron-Faust, MPH

Even with health insurance, some patients with rheumatoid arthritis (RA) may not be adequately treated. This news comes from an analysis of a large nationwide pharmaceutical claims database.

Analysis of claims data from 4.66 million American adults treated for RA between January 2005 and September 2008, finds that only two-thirds of patients with newly diagnosed disease received DMARD therapy during the first year after their diagnosis.

And 28% received no DMARDs at all, just treatment for symptoms.

Those patients receiving only symptomatic relief tended to be older and had more co-morbidities and contraindications to methotrexate, according to the industry-sponsored retrospective cohort study.

At the same time, the authors observe, “this population was arguably underserved because 38% of this inception cohort did not see a rheumatologist in year one, and 15% never saw one over a median of 2.3 years of follow-up.”

Although one-fifth did receive biologics within 12 months, there was extensive medication switching among the group, and a relatively rapid decline over time in patients who stayed on the drugs.

The analysis reveals a somewhat lower incidence of RA than other population studies, but a similar age and gender adjusted prevalence of RA (0.63% overall, and 0.33% in men and 0.92% in women).

While the data lack supporting clinical information, such administrative databases can reflect actual treatment patterns in daily clinical practice. The same patterns of treatment of RA have been seen in other studies, they note.

The study was aimed at determining whether physicians were following current American College of Rheumatology RA treatment guidelines.

There could be a number of reasons for the apparent under-treatment of patients, the study authors speculate: lack of physician awareness of, or disagreement with, treatment guidelines; and determinations that patients were too old, their disease too mild, or there were contraindications for therapy.

Patients may have also wanted to avoid drug treatment due to adverse effects or costs, they add.

Within 12 months after their diagnosis, 65%, 64%, and 20% of the incident cohort (those without an apparent prior diagnosis of arthritis) had been prescribed corticosteroids, non-biologic DMARDs, and TNF-inhibitors, respectively.

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.