Let me help you meet awesome people and earn at the same time with UBER Drive Now $1000 bonus from Uber for first time driver Car must at least be 2008 or newer model. Have a smart phone. Learn use…

Source: Receive $1000 bonus as Uber driver if you are laid off bay area workers

If you have trouble hearing, or notice that your hearing is not as good as it used to be, listen up.

Age-related hearing loss may be retrievable, according to Dr. Jonathan Wright, MD, medical director of the Tahoma Clinic in Washington.

Bioidentical hormone aldosterone

By supplementing three patients with the bioidentical hormone aldosterone, all of the men who were either losing their hearing or who had lost a lot of their hearing  were able to regain much of what had been lost.

In one case, an 87-year-old man who was diagnosed with hearing loss in 1994 was found to have low aldosterone levels. After six weeks of taking aldosterone, the man visited his audiologist and found that his hearing had increased 30-50 decibels in one ear, and 20-30 in the other. His ability to discriminate words from a noisy background also increased significantly.

An animal study has also suggested that the hormone aldosterone was able to restore hearing.

This process of using bioidentical hormones to restore hearing is actively going on at the Tahoma Clinic, which is presently the first and only place in the United States that is using aldosterone to restore hearing.

• My personal interview with Dr. Jonathan Wright, November 24, 2007

Opoid narcotics pain killers have morphine. The same morphine in sublingual form is given to hospice client with few weeks to live.

Payment Options — Knowing that there are specialized care options for individuals with dementia is helpful. Since custodial care, by definition, does not need to be provided by a skilled professional, most insurance, including Medicare, will not pay for such care. This becomes quite a quandary for many individuals. For those with financial resources, they can pay privately for the type of care that is necessary. But what happens when the financial resources have been exhausted? How do those individuals without financial means obtain the necessary care? There are some options.

One option is long-term care insurance. Long-term care insurance policies are not standardized like Medicare supplement insurance. These policies can cover a wide continuum of care and must be purchased prior to the onset of a chronic illness.

There are a large variety of companies selling policies with multiple combinations of benefits and coverage. Therefore, when shopping for long-term care insurance policies, it is imperative that:

• You have thoroughly thought about the type of care that you may desire in the future
• It is fully understood what is being purchased and what the policy will and will not cover. For example, some policies will only cover nursing home care while others will cover home health care and assisted living care as well. In addition, some policies may often cover care for a specified amount of time (such as 3-5 years) and then the policy will expire.

Another option is seeking assistance from state insurance programs such as Medicaid. Many state insurance programs will cover custodial care in nursing facilities as well as some care in the home and adult family homes. Eligibility for these programs and what types of care they will cover varies between states. To determine eligibility guidelines and the type of care that is covered, contact your local social services office, Area Agency on Aging.

It is wise to speak with an elder law attorney or a financial planner to plan for the future and to determine which options are the most feasible. It is important to know and understand the financial situation so that resources can be managed and budgeted over an extended period of time.

How to Determine the Most Appropriate Care Options – The decision-making processes are often times left to the caregiver. The chosen options must meet the care needs of your loved one, but they must meet your needs as well. Although you want the individual that you are caring for to be as independent as possible, they must be safe and secure. You may want to ask yourself the following questions when faced with a decision:

• What type of services and assistance do you, the caregiver, need? What types of services will provide you with the most efficient, affordable and necessary assistance?
• What types of assistance and care does the individual you are caring for need? Some areas in which an individual may need assistance with are:
  • assistance with financial management and banking needs
  • bathing
  • dressing
  • health maintenance such as taking medications as prescribed
  • housekeeping
  • meal preparation
  • mobility
  • supervision
  • toileting
  • transportation
• Do you have a clear understanding about the individual’s physical, emotional and cognitive strengths and limitations?
• Do you understand the individual’s preferences regarding the type of care they would like to receive?
• Are you able to respect their preferences even if they are in conflict with yours as long as the individual will remain safe and have their needs met?
• Do you have a good understanding of the individual’s financial situation and the type of care and services they can reasonable afford?
• Is the individual involved as much as possible with the decision making process? Are all individuals that may be impacted by the decision involved in the process?
• ————–
• 
• Call 408-854-1883 , motherhealth@gmail.com for flexible payment options for your parents with AD or PD in the bayarea.
• Sometimes, family members can take turns with 2-3 caregivers from our agency to provide 24/7 care for homebound seniors.

In Canada, you can hire a foreign live-in caregiver. When my sister was in Singapore, she also completed some paperwork from the government of Singapore. In the USA, it would be impossible to hire a foreign live-in caregiver but you can hire a foreign nanny for your children.

To hire a live-in caregiver in the bayarea, contact Motherhealth caregivers at 408-854-1883 and email motherhealth@gmail.com
We will help you search for a caregiver that matches your needs.

There are questions you need to answer for your parents who need a live-in caregiver such as:

• Describe the healthcare needs of your parents with Alzheimer’s or Parkinson’s
• Are they wheel chair bound? Are they under hospice care?

I want to hire a foreign worker as a live-in caregiver in Canada. What steps do I take?

Before investing time and money, learn about the conditions of the Live-in Caregiver Program. Be sure it is the best way to meet your needs.

You must first try to hire a Canadian citizen or permanent resident in the available job. When you apply to Employment and Social Development Canada (ESDC) for permission to hire a foreign worker, you will be asked to show what efforts you made in this regard.

If you have been unable to hire a Canadian or permanent resident, your next step is to apply to ESDC for what is known as a Labour Market Impact Assessment (LMIA), which confirms that there is no Canadian worker available to do the job. If ESDC issues you a positive LMIA, you are then authorized to hire a foreign worker.

It also tells you which documents you must give your future employee so that he or she can apply for a work permit through a Canadian visa office outside Canada.

You are responsible for finding a foreign live-in caregiver. To do so, you can use advertisements, personal contacts or hiring agencies.

When you have found a foreign live-in caregiver you want to hire, you must first contact Employment and Social Development Canada (ESDC). If your future employee applies for a work permit and meets the program’s requirements, he or she will receive a work permit. The approval process could take several months. Check the latest information on CIC’s processing times. Your caregiver cannot work for you until CIC approves a work permit showing your name as the employer.

Natural health products that inhibit angiogenesis: a potential source for investigational new agents to treat cancer—Part 2 S.M. Sagar, MD,* D. Yance, MH,† and R.K. Wong, MD* * Juravinski Cancer Ce…

Source: Natural cancer cures

Natural health products that inhibit angiogenesis: a potential source for investigational new agents to treat cancer—Part 2

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2. MULTISTEP ACTIVITY OF PHYTOCHEMICAL COMPLEXES DERIVED FROM HERBS

2.1 Targeting Alternative Angiogenesis Pathways

The adipocytokines—polypeptides produced by adipocytes—have autocrine, paracrine, and endocrine activities, and are associated with obesity, hyperinsulinemia, and chronic vascular disease as well as with the development of cancer ¹. The adipocytokines include vascular endothelial growth factor (vegf), hepatocyte growth factor (hgf), leptin, tumour necrosis factor alpha (tnfα), heparin-binding epidermal growth factor, insulin-like growth factor, and interleukin-6 (IL-6). All can promote angiogenesis.

Curcumin (from turmeric) and epigallocatechin-3 gallate (egcg, from green tea) can inhibit aminopeptidase-N (CD13), a member of the matrix metalloproteinase family that is implicated in the angiogenic switch process ^2–4. Curcumin and egcg can also interfere with the expression of vegf by suppressing a series of activities that promote angiogenesis. These angiogenic pathways include production of transforming growth factor beta (tgfβ), amplification of cyclooxygenase-2 (cox-2) and epidermal growth factor receptor (egfr), aberrant expression of src, and amplification of nuclear factor kappa-B (nf-κb) signalling. Curcumin, grape seed extract, and green tea constituents may also interfere with endothelial cell function by inhibiting the engagement of specific integrins ^5,6. These phytochemicals interact at multiple levels to suppress the inflammatory, hyperproliferative and transformative processes that constitute carcinogenesis.

2.2 Targeting EGFR (HER1)

In many human tumours, egfr is overexpressed. Such overexpression is associated with more aggressive disease, relative resistance to cytotoxic chemotherapy, and a poorer prognosis. Activity of egfr induces angiogenesis ⁷. Blockade of egfr reduces angiogenesis and cell proliferation ⁸. Monoclonal antibodies have been developed to block the receptor or the linked intracellular signalling system ^9–15.

Epidermal growth factor (egf) stimulates urokinase-type plasminogen activator (upa) expression, which can promote angiogenesis. Genistein (an isoflavone constituent of soy) and curcumin (a constituent of turmeric) both inhibit the effects of egf ¹⁶. In cell cultures, genistein and curcumin inhibit egf-stimulated urokinase production and phosphorylation of egfr. Both botanicals also inhibit protein tyrosine kinases, which could stimulate the enhancement of upa levels induced by tgfβ ¹⁷.

Other natural health products that can block activity of egfr include resveratrol ¹⁸ and quercetin ^19–21.

2.3 Targeting HER2/neu

The HER2/neu gene (formerly known as c-erbB-2) is amplified in more than 30% of patients with breast cancer. It is linked to highly aggressive tumours with a poorer prognosis. Overexpression of HER2 is also seen in a significant proportion of patients with other cancer types, including non-small-cell lung cancer, ovarian cancer, prostate cancer, and gastric cancer, in which it may predict a worse outcome ^22–26. Amplification of the HER2 gene correlates with higher levels of angiogenesis ²⁷.

Herceptin (Genentech, San Francisco, CA, U.S.A.) is a drug that inhibits HER2/neu. It is usually administered adjunctively with cytotoxic chemotherapy. The activity of Herceptin may be further enhanced by oleic acid ²⁸. Emodin, a natural constituent of Polygonum multiflorum and aloe, inhibits HER2/neu expression and is toxic against cancer cells, but nontoxic for normal cells ²⁹.

2.4 Targeting Inflammatory Pathways: COX-2 and NF-κB

Prostaglandins are autacoids derived from arachidonic acid via the cox enzymes. They include prostacyclin, thromboxane, and prostaglandin E types 1–3. A role for arachidonic acid–derived prostaglandins in the process of angiogenesis is now established through in vitro assays. Prostaglandin E2 is a potent inducer of angiogenesis. A correlation exists between cox-2 expression and angiogenesis ³⁰. Neovascularization is blocked by cox-2 antagonists ^31–36.

The cox-2 and lipoxygenase (lox-5) products of omega-6 fatty acid metabolism may exert stimulatory effects on cancer progression including angiogenesis. The omega-3 fatty acids and some pharmacologic inhibitors of eicosanoid biosynthesis antagonize these effects ^37–41. Large amounts of omega-3 fatty acids [eicosapentaenoic acid (epa) and docosahexaenoic acid] are found in cold-water fish oils. Liquorice contains glycyrrhizic acid and polyphenols that inhibit cox-2, lox-5, and protein kinase C (pkc) and also downregulate egf ⁴².

The nf-κb family consists of closely related protein dimers that bind to a common sequence motif in dna called the κb site. The nf-κb inducible transcription factor is increased in tissue inflammation, cell proliferation, and cancers. Nuclear factor kappa B induces overactivation of the cox enzymes and is associated with increased angiogenesis ^43–46.

The cox enzymes are expressed in most normal tissues. The cox-1 enzyme synthesizes non-inflammatory prostaglandins such as prostaglandin E1. In contrast, cox-2 is amplified as part of the inflammatory response and produces prostaglandins such as prostaglandin E2, which may induce uncontrolled cell proliferation and carcinogenesis.

Nuclear factor kappa B may be amplified by growth factors, including tgfβ and basic fibroblast growth factor. Besides nf-κb, other transcription factors, such as activator protein-1 (ap-1) and IL-6, can stimulate cox-2 transcription. Activator protein-1 also promotes the metastatic phase of tumour cells.

Angiogenesis mediated by cox-2 also has a role in the progression of pre-neoplastic lesions to the invasive phenotype ^47–50. Conventional cancer therapies—such as radiation, surgery, and chemotherapy—may induce cox-2 amplification as part of the inflammatory response ⁵¹. The significance of this induction is unclear, but it could hypothetically reduce therapeutic gain.

Several phytochemical derivatives are potent inhibitors of nf-κb. These include resveratrol, piceatannol, curcumin, egcg, 6-gingerol (ginger), ursolic acid (holy basil), and ginseng ^52–56. Many botanical cox-2 inhibiting agents block the amplified activity of the transcription factor nf-κb without affecting its normal function.

A variety of natural health products can specifically inhibit the cox-2 enzyme and could play a role in reducing tissue toxicity and improving tumour control when used alongside therapies such as radiotherapy, chemotherapy, and surgery (Table I) ⁵⁷. A botanical that protects an organism from the adverse effects of an intervention is termed an adaptogen. Panax ginseng and curcumin are adaptogens that inhibit cox-2 and that have anti-angiogenic activity derived through the inactivation of nf-κb ^55,58–61

Table I

Natural health products that inhibit cyclo-oxygenase-2 activity ⁵⁷

2.5 Targeting Protein Kinases

Oncogenes that encode protein kinases may contribute to the development of cancer. In normal cells, protein kinases are involved in signals between the cell membrane and the nucleus, regulating progression through the cell cycle. Protein kinases control these processes by activating other messenger proteins that can influence cell proliferation.

Mutated kinase genes have been found in a number of malignancies, including chronic myelogenous leukemia and breast and bladder cancers. The mutated kinases can contribute to the development of cancer. In many tumour cells, protein kinases are permanently turned on, forcing the cell into constant division. Examples of abnormal kinases are the abl, src, and cyclin-dependent kinases. The kinases may be amplified or permanently switched on by mutations in the control regions of their genes. A commonly overproduced kinase in cancer is egfr.

Numerous phytochemicals are reported to interfere with cell signalling and may reverse the adverse effects of protein kinase overactivity. Some botanicals with cox-2 inhibitory activity target the intracellular signalling molecules ^62,63. Inhibition of specific protein kinases suppresses angiogenesis ^64–69.

Carnosol and ursolic acid are compounds found in Ocimum sanctum (holy basil) and Rosmarinus officinalis (rosemary) ⁷⁰. They inhibit the activity of the tyrosine kinases and ornithine decarboxylase ⁷¹. Carnosol also reduces nf-κb ⁷² and the anti-apoptotic protein Bcl-2 ⁷³. Genistein and daidzein (isoflavones found in soy) are specific inhibitors of tyrosine kinases ⁷⁴.

Many phytochemicals appear to selectively react with the regulatory centre of pkc. Curcumin, vitamin E, green tea (catechins), resveratrol, Ganoderma lucidum, and liquorice can inhibit pkc activity ^42,75–77

2.6 Targeting the Bcl-2 Protein

The signalling protein Bcl-2 plays a key role in the process of controlled cell death called apoptosis, which is necessary to eliminate aged or damaged cells. The Bcl-2 protein is normally found in the mitochondrial membrane, where it regulates the release of cytochrome C. The latter protein can trigger a series of enzymes (caspases) that lead to cell death ^78–81. High Bcl-2 levels are associated with most types of human cancer and block the release of cytochrome C. They appear to be a contributor to both inherent and acquired resistance to anticancer treatments. The BCL2 and TP53 genes regulate vegf-mediated angiogenesis ⁸²

Curcumin and green tea extract inhibit BCL2 expression ^83–85. Scutellaria baicalensis contains the phenolic compounds baicalin, baicalein, wogenin, and oroxylin. These constituents inhibit BCL2 overexpression, plus COX2 gene expression and nf-κb activation ^86,87. Hibiscus protocatechuic acid is a phenolic compound isolated from the dried flower of Hibiscus sabdariffa L.; it inhibits Bcl-2 activity ^88,89. Other inhibitors of Bcl-2 include epa from fish oil ⁹⁰, a lectin extract of Viscum album (mistletoe) ⁹¹, 6-gingerol ⁹², grape seed extract ⁹³, echinocystic acid (a triterpene found in ginseng and other Asian herbs) ^94,95, parthenolide (a sesquiterpene lactone found in feverfew) ⁹⁶, and beta-lapachone (a quinone obtained from the bark of the lapacho tree) ^97–99.

2.7 Targeting Coagulation Pathways Associated with Angiogenesis

In some clinical trials, anticoagulation drugs have been associated with a reduction in metastases ^100–102. In Chinese medicine, destagnation herbs are traditionally thought to overcome blockages of qi and blood. Laboratory evidence now suggests that these herbs may have anti-angiogenic and anticoagulation properties ^103–105. A randomized placebo-controlled trial showed that the addition of “destagnation” herbs (including Salvia miltiorrhiza and Angelica sinensis) to radiotherapy doubled both the local control and the survival rate in patients with nasopharyngeal cancer ¹⁰⁶.

Are stem cells epigenetic? By Sydney Strupp Now, note the diagram above. See the blue ball on the top? That represents an iPS cell, an undifferentiated cell that can be determined to become anythin…

Source: Cell types, methylation cycle, Anti-aging

Are stem cells epigenetic? By Sydney Strupp

Now, note the diagram above. See the blue ball on the top? That represents an iPS cell, an undifferentiated cell that can be determined to become anything. Stem cells are like this cell-many different cell types can come from it. iPS cells are typically seen in a developing zygote. They have a very “clean” DNA, meaning not a lot of epigenetic markers on it until it becomes determined to be a certain kind of cell by cellular determinants in the cytoplasm. So, the iPS cell now spurred by the determinants, travels down the slope into one of the four pockets, becoming that cell. To become that cell type, proteins add methyl groups to certain regions of the DNA and suddenly, by the grace of epigenetics, the unspecialized cell becomes specialized.

The important thing to understand from my rambling nonsense is that all cells start and end with the same DNA, it’s just altered via epigenetic markers. Your kidney cells have the same DNA as your heart. Thankfully, the methyl additions to your DNA are permanent enough to stop a kidney cell from developing in your heart. That’s because heart cells are so specialized uniquely, using an entirely different region of DNA (mostly) that unless the cell had the correct determinants in it’s cytoplasm, the proteins would never add methyl groups for the cell to become that type of cell. They would be at the very bottom of the trough, in one of the deepest pits.

Now, finally getting back to your question. Are stem cells epigenetic? Well, they’re more like the lack of epigenetics. They have very naked DNA that is waiting to be methylated into many different types of cells. They are waiting for the right determinants to “roll them down the hill” into the cell of choice.

Increasing Methylation , one of anti-aging factors

The Methylation Cycle, preventing fatigue and aging

Rich van Konynenburg’s idea is that ineffective methylation is a major cause of fatigue. There are many possible reasons but those that he’s identified for which methylation is essential are:

• To produce vital molecules such as Co Q-10 and carnitine.
• To switch on DNA and switch off DNA. This is achieved by activating and deactivating genes by methylation. This is essential for gene expression and protein synthesis. Proteins of course make up the hormones, neurotransmitters, enzymes, immune factors and are fundamental to good health. When viruses attack our bodies, they take over our own DNA in order to replicate themselves. If we can’t switch DNA/RNA replication off then we will become more susceptible to viral infection.
• To produce myelin for the brain and nervous system.
• To determine the rate of synthesis of glutathione which is essential for detoxification.
• To determine the rate of synthesis of glutathione which is an essential anti-oxidant as glutathione-peroxidase. Furthermore oxidative stress blocks glutathione synthesis – yet another vicious cycle!
• To control sulphur metabolism of the body, not just glutathione but also cysteine, taurine and sulphate. This is an important process for detoxification.
• As part of folic acid metabolism. This also switches on synthesis of new DNA and RNA.
• For normal immune function. The methylation cycle is essential for cell mediated immune function and blockages here will mean that infections will not be adequately dealt with. I know this clinically because many patients tell me that once they get on to their B12 injections (an essential co-factor for methylation) this seems to protect them from getting infections.

The overall effect here is that if the methylation cycle doesn’t work, the immune system malfunctions, the detoxification system malfunctions, our ability to heal and repair is reduced and the anti-oxidant system malfunctions.

The Bio-chemistry

(You can ignore this bit if you like because it’s not essential to know but it’s interesting.)

There are four cornerstones to the methylation cycle and on each cornerstone sit four molecules namely homocysteine, methionine, S-adenosylmethionine (SAMe) and S-adenosylhomocysteine. Each of these molecules leads into the next one by means of enzymes. The important co-factors that allow this to happen are the B vitamins such as folic acid, vitamin B12 and vitamin B6. In converting from S-adenosyl methionine into S-adenosyl homocysteine, a methyl group is given up and this can be used to stick on to other molecules – hence the name, the methylation cycle.

However, there is a particular bio-chemical glitch here. In order for the methylation cycle to work these B vitamins have to be in their activated form, namely methylcobalamin, folinic acid and pyridoxyl-5-phosphate. In order to get cobalamin into methylcobalamin, the methylation cycle has to be working. So if this cycle has crashed completely, the body can’t make methylcobalamin in order to get it up and running again. Since this cycle is so fundamental to other biochemical cycles including trans-sulphuration and folate metabolism, it can’t change the vitamin B6, folic acid and cobalamin into the active forms necessary for the methylation cycles to work.

This means that in order to get this cycle up and running initially we have to prime the pump with the activated vitamins, but hopefully once the methylation cycle is up and running, it can function on the vitamins in normal states.

Dr Myhill wrote:

The important cycles which I know to be major players include blood sugar wobbles, allergy problems, sleep cycles, mitochondrial function, anti-oxidant status, the NO/OONO cycle, thyroid and adrenal hormones cycles and de-toxification

We don’t have a simple test to see how well the methylation cycle works. What we can do is measure levels of homocysteine and SAMe

The Methylation Cycle – which supplements to take to support

This is the package of supplements to support the methylation cycle. It needs to be taken in addition to everything else, i.e. the standard nutritional package (multivits, multiminerals, EFAs, vits C + D) and the mitochondrial rescue package (D-ribose, acetyl-L-carnitine, CoQ10, etc.)! But the methylation package will change with time because as the methylation cycle starts to work again, it will start to stand on its own feet. Everyone”s package will be a bit different depending on how poorly their cycle is working. One day we will have the biochemical tests to tailor make each package for each person, but until then I suggest the following regime for those sufferers who have been taking vitamin B12 in oral form (as either hydroxocobalamin or cyanocobalamin):

For two months a daily dose of

•  Methylcobalamin 1 mg sublingually
•  Methyltetrahydrofolate 800mcg (ActiFolate)
•  Pyridoxal-5-phosphate 100mgs (50mgs twice daily)
•  Glutathione 250mgs daily
•  Phosphatidyl Serine 200mgs (100mgs twice daily) – BioCare

If you are better – fine! If you are worse – it may be the reaction to the methylation package because it may cause an acute detox reaction (see below). Slow down the regime – take smaller amounts of the supplements and build up slowly. If you are unchanged – swap the sublingual B12 for injected B12 ie:

Daily subcutaneous injections methylcobalamin 0.5mgs (this is a bit more expensive than cyanocobalamin). Some CFSs will not respond clincially until 5mgs daily is injected. B12 is very safe with no known toxicity- as a colleague commented – the only way you could kill yourself with B12 would be to drown in the stuff! I would prefer people to start with this regime but I know many do not fancy the idea of injections – actually I am a wimp too, but they are easy and almost painless.

•  Methyltetrahydrofolate 800mcg (ActiFolate)
•  Pyridoxal-5- phosphate 100mgs (50mgs twice daily)
•  Glutathione 250mgs daily
•  Phosphatidyl Serine 200mgs (100mgs twice daily) – BioCare

If you are better – fine! If you are worse – it may be the reaction. If you are unchanged, add in:

•  Tri-methylglycine or TMG (not to be confused with betaine hydrochloride, so always ensure that you are taking pure-grade TMG)
•  Lecithin (phosphatidyl choline) and Phosphatidyl Ethanolamine.
•  S-adenosyl methionine (SAMe) directly as a supplement 400mgs daily

I have seen and talked to families in California (bayarea) and found out how they will vote for the Presidential elections. Parents will vote for Hillary and their children will vote for Bernie San…

Source: Why parents are voting for Hillary Clinton and children are voting for Bernie Sanders

I have seen and talked to families in California (bayarea) and found out how they will vote for the Presidential elections.

Parents will vote for Hillary and their children will vote for Bernie Sanders.

The parents have an income of over $250k per year and are afraid to be taxed more by Bernie while the children are for Bernie because he can change the system with free college and health care system.

The arena is packed by supporters of Bernie Sanders yet the media is not writing about it.

The parents should know that many future policies on health care, drug costs and nursing homes will affect them.

Food and absorption of drugs/supplements

 Food and its constituents may have a significant effect on both the rate and extent of absorption of drugs after oral administration. Understanding the effect of meals on medicines enables health professionals to advise patients about taking medicines with or without food. Co-administration of drugs with food generally delays drug absorption. However, meals may have a variable effect on the extent of absorption – depending on the characteristics of the meal, the drug and its formulation. Some drugs have strict guidelines about when they should be taken in relation to meals. Generally, patients should be advised to take their medicines consistently at the same time with respect to meals.

 Bioavailability and drug interactions with food

 Understanding the possible clinical implications of taking medicines with or without a meal is important for achieving quality use of medicines. Although the effect of food is not clinically important for many drugs, there are food-drug interactions which may have adverse consequences. Often these interactions can be avoided by advising the patient to take their medicines at the same time with respect to meals.

The effect of food on absorption

The formulation of a drug influences its absorption. Food can affect both the rate and extent of absorption (Table 1).

Rate of absorption

Meals slow down gastric emptying and this can delay drug absorption. The composition of the meal influences the rate of gastric emptying – high fat meals lead to delayed gastric emptying. A delay in the drug reaching the small intestine can delay its subsequent absorption into the systemic circulation. Based on these observations, oral administration of a medicine under fasting conditions is often recommended when rapid absorption (and hence rapid onset of therapeutic effect) is needed. For most medicines, especially those used for chronic conditions, a delay in the onset of absorption is of no clinical consequence as long as the amount of drug absorbed is unaffected.

Extent of absorption

Food has the potential to either increase or decrease the extent of drug absorption. Understanding food-drug interaction mechanisms enables the clinician to provide appropriate advice to patients about taking medicines with respect to the timing and composition of meals.

The effect of food depends on the physicochemical and pharmacokinetic characteristics of the drugs.1 The clinical significance of the effect will in turn depend on the pharmacodynamic characteristics of the drug. For example, the poorly water soluble antiretroviral drug saquinavir should be taken with food to allow bile enhancement of its dissolution which then facilitates absorption. The extent of absorption is more than doubled by taking saquinavir after a full cooked breakfast. Taking saquinavir on an empty stomach reduces its bioavailability and could lead to therapeutic failure.1

Delayed gastric emptying after a meal and the associated gastric acid secretions can reduce the bioavailability of some medicines that are acid labile. The constituents of a meal may also specifically interact with drugs (Table 2). Calcium and other cations in food can form insoluble chelates with some medicines preventing their optimal absorption. Bisphosphonates are therefore recommended to be taken with plain water to prevent the formation of chelates which significantly reduce bioavailability.

Source:

 Aust Prescr 2006;29:40-2 | 1 April 2006 | http://dx.doi.org/10.18773/austprescr.2006.026

Andrew McLachlan and Iqbal Ramzan, Faculty of Pharmacy, University of Sydney, NSW

Comments:

Take your digestive enzymes and acidophilus before a meal to increase bioavailability and be present in our body before we ingest food so that these enzymes and supplements can be more beneficial. Do take fat-rich meal with Vit E, D, K and A.  And always have Vitamin C rich foods with meals as it helps in the absorption of nutrients.

Do not eat/drink grapefruit when taking any meds/drugs as it doubles their potency.