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The holiday season is just around the corner – the time of year when we find ourselves surrounded by sweet treats and comfort foods. It becomes too easy to over-indulge, and you find yourself craving that extra slice of turkey or pumpkin pie or reaching for a few more holiday cookies.
It happens to the best of us this time of year. To avoid making the same New Year’s resolution about getting back to the gym and shedding that extra winter weight, here are some strategies to help control holiday cravings this season.
Hunger versus Craving
Before diving too deep, it’s important to understand the difference between real hunger and a craving. Below are some common ways to identify whether you’re really hungry or just experiencing a craving.
Hunger:
A craving:
Bottom line: A craving has more to do with what your mind wants – while hunger has more to do with what your body needs.
Understand your cravings
As you probably know – a craving has little to do with actual hunger. Instead, a food craving is likely caused by biological and psychological factors. The first step to overcome cravings is to understand the cause. Once you identify the cause, it’s easier to manage your craving.
Here are a few of the most common causes of food cravings.
Your mood: Chronic stress, anxiety, and low serotonin levels contribute to cravings. For example, stress causes a spike in your cortisol level, and that can lead to a craving for sweet, sugar-packed carbs. A bad or sad mood can also mentally and physically affect cravings. Because sugar consumption or binging on your favorite comfort foods releases serotonin (a neurotransmitter that regulates mood, appetite, memory, and social behavior), your brain begins to crave these treats so it can release this “feel good” chemical again and again.
What you can do: Try testing your stress hormones to determine if your stress levels are too high, or try incorporating a supplement that helps manage stress and sugar cravings by boosting serotonin levels.* If you’re unsure what stress supplement might be best for you, then take our stress quiz. [link to it when it’s up]
You are not getting enough sleep: We get energy from two things – sleep and the food we eat. If you aren’t getting enough of the first one, that is, if you have poor sleep habits or suffer from poor sleep quality, then your body could compel you to eat more as a way to get more energy.
What you can do: Check the hormones that regulate your sleep cycle to find out if sleep is a factor for your cravings. If it is, then try to get better quality and more consistent sleep. Set a sleep schedule to wake up and go to bed at the same time each day. You could also consider using a supplement, such as melatonin, to support a regular sleep schedule.*
Nutrient deficiency: One sneaky cause of food cravings could be suboptimal nutrient or electrolyte levels in your body – such as magnesium, chromium, zinc, sodium, omega-3 fatty acids, or B vitamins. Some of these imbalances can manifest themselves as sugar cravings and others as salt cravings. An iron deficiency can lead to feeling fatigued and can cause you to crave sugary carbs as a quick way to perk up. Low iron is easily detected with a simple blood test.
What you can do: Incorporate foods high in these nutrients into your diet. Or use a highly absorbable multi-mineral supplement, a full-spectrum B-complex for stress, or an electrolyte formula. Chromium Picolinate has a highly absorbable form of chromium, which is often lacking in our modern diets. This essential mineral supports healthy blood sugar levels and helps lessen carbohydrate cravings.*
Dehydration: One common cause of food cravings is a lack of water. Because the body interprets hunger and thirst in a similar way, it can be hard to tell the difference. An easy solution is to drink a big glass of water and wait. If the craving goes away, it’s likely you were just dehydrated.
What you can do: Ensure you drink at least eight 8-ounce glasses of water a day.
Some general guidelines this holiday season
Now that you have a better idea of what can cause a craving, here are some helpful habits to begin curbing and controlling them.
Mood disorders are mental health issues that primarily affect a person’s emotional state, in which a person experiences long periods of extreme happiness, extreme sadness, or both.1 In the fifth addition of The Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the list of mood disorders and their diagnostic criteria are exceedingly lengthy; but the most common include major depression, dysthymia, bipolar disorder, seasonal affective disorder (SAD), and depression related to an illness, substance abuse or medication.2 For simplicity of this article, I will refer to these issues collectively as mood disorders unless otherwise indicated.
The 2001-2003 National Comorbidity Survey Replication shows an estimated 9.7% of US adults (anyone over 18) had any mood disorder in the past year, with a higher prevalence in females (11.6%) than males (7.7%); and an estimated 21.4% of US adults will experience a mood disorder at some point in their lives.3 Please note that these figures are a combination of mood disorders; frequently updated individual statistics may be found by accessing the National Institute of Mental Health Statistics website at https://www.nimh.nih.gov/health/statistics/index.shtml.
Depression alone affects more than 300 million people worldwide.4 Bipolar disorder affects more than 60 million, and SAD can affect up to 10% of the population, depending on geographical location.5 The direct and indirect costs of these health issues are immense. For example, in 2008, the World Health Organization (WHO) ranked major depression as the third leading cause of burden of disease worldwide and projected that the disease will rank first by 2030.6 In 2015, it was estimated that bipolar I disorder (BDI) total costs were $202.1 billion (US dollars), an average of $81,559 per affected individual.
Sadly, the aforementioned numbers of afflicted individuals, as well as cost burden, are likely underestimates because many of the individuals that struggle with mood disorders go undiagnosed. At times, they may be reluctant to seek help due to the social stigma associated with these conditions. In practice, mood disorder detection, diagnosis, and management also pose many challenges for clinicians because of various presentations, unpredictable course and prognosis, as well as variable response to treatment.7,8
There is an urgent need for safer and more efficacious alternatives to medications. Medications certainly have their role in mood disorders, when used judiciously. It has been well established in mild to moderate depression, for example, that medications are no more effective than placebo.9 In manic and depressive states of bipolar disorder, the data is mixed on how efficacious medications really are.10
The extensive laundry list of side effects of mood disorder medications is so vast, it makes one’s head spin. In clinical practice, it seems the side effects tend to be so intolerable for patients, they would many times rather suffer from their illness than deal with the negative consequences of the medications. Antidepressants, anxiolytics, stimulants, antipsychotics and mood stabilizers are typically used with mood disorders; but a full discussion of their efficacy and potential side effects is beyond the scope of this article.
To better understand mood disorders and provide more effective treatment interventions, it is beneficial to look at underlying etiologies, risk factors, and genetics (encompassing family history). Each particular mood disorder has its own unique set of etiologies, but commonalities amongst all of them include brain structural changes (not yet well understood) compared to those without mood disorders, neurotransmitter alterations, and hormonal imbalances. Risk factors include low self-esteem, being highly self-critical, traumatic and stressful events (e.g., physical or sexual abuse, loss of a loved one), comorbid mental disorder (e.g., schizophrenia or anxiety disorders), alcohol and recreational drug abuse, chronic illness, and side effects of certain medications (e.g., sleeping pills and anti-hypertensive drugs).11
An enormous risk factor is genetics12 and even epigenetics.13 Research into the role single nucleotide polymorphisms (SNPs) play in mood disorders has exploded in the last 15 years or so and offers promise to help improve people’s lives through nutritional and botanical interventions.14,15 Indeed, even pharmacogenetic testing is finally becoming more mainstream in clinical practice, offering safer, more specific, personalized pharmaceutical options.16-18
A comprehensive, integrative approach to mood disorders works very well in clinical practice.19 This may include all or most of the following: lifestyle and dietary modifications, constitutional homeopathy, botanical medicines, nutraceutical support, psychotherapy, and occasionally pharmaceutical interventions. Again, given space limitations, this article will focus on evidence-based botanical and nutraceutical interventions.
Studies are consistent that up to half of all individuals diagnosed with a mood disorder use one or more complementary and alternative medicine (CAM) therapies.20,21 It has been shown that diet,22 exercise,23 sleep, a strong supportive social network, and low stress environment reduce relapses in mood disorders.24 Even targeting the proverbial “gut microbiome” can have a tremendous positive impact!25,26
Given all of the aforementioned information and dire need of safe and effective alternatives, are there really any nutraceutical and/or botanical interventions that work? The answer is yes, definitely.
Vitamin B12 (cobalamin) is involved in DNA synthesis, red blood cell formation, homocysteine metabolism, and synthesis of S-adenosylmethionine (SAMe). It also is heavily involved in the proper function of the nervous and immune systems.27 Observational studies have shown that as many as 30% of patients hospitalized with depression are deficient in this vitamin.28 Depression can be induced by B12 deficiency, even with normal hematological and blood parameters,29 so a therapeutic intervention of 1000 mcg (1 mg) daily, orally, has been suggested.30 The forms of B12 in these studies have varied.
It has been shown that individuals with psychiatric conditions either have impaired transport across the blood-brain barrier and/or an accelerated catabolism, hence the need for increased requirements.31 When these individuals were treated with a therapeutic trial of B12, clinical improvement was noted.32
Folate is a generic term referring to both natural folates in food and folic acid (the synthetic form used in many supplements and fortified food). Folate is critical in the synthesis of DNA and RNA, several amino acids, methylation reactions, homocysteine and B12 metabolism, and assists in the proper functioning of the central nervous and immune systems.33
Like B12, low red blood cell folate levels have been detected in 15–38% of adults diagnosed with depressive disorders.34 Efficacious doses have ranged from 200 mcg to 15 mg of folic acid, along with medication(s), depending on the mood disorder.35,36 Do note, most trials have been conducted on folic acid, not its biologically active forms of 5-methyltetrahydrofolate (5-MTHF, the major circulating form in the body) and 5,10-methylenetetrahydrofolate. In individuals with methylene-tetrahydrofolate reductase (MTHFR) polymorphisms and/or on medications that inhibit dihydrofolate reductase (by reducing interactions), along with those having compromised gastrointestinal function, folinic acid and 5-MTHF may be the preferred forms.37,38
Vitamin B6 (pyridoxine, pyridoxal and pyridoxamine) and its coenzyme form, pyridoxal 5’-phosphate (PLP), are essential to over 100 enzymes, affecting lipid, amino acid, and carbohydrate metabolism, along with the action of steroid hormones.39 It cannot be synthesized in the body and must be obtained from the diet. In the brain, PLP is necessary to metabolize serotonin from tryptophan and dopamine from L-3,4-dihydroxyphenylalanine (L-Dopa). Other neurotransmitters and amino acids that are PLP-dependent include glycine, D-serine, glutamate, histamine, and γ-aminobutyric acid (GABA).40 PLP also plays a role in the metabolism of homocysteine.41 Typical dose ranges are from 10 to 200 mg/day, but anyone taking more than 200 mg/day should be monitored for neurotoxic symptoms.42
Vitamin D3 (cholecalciferol) is a fat-soluble vitamin that functions as a hormone precursor. It is biologically inactive and must first be hydroxylated in the liver to 25-hydroxyvitamin D (25[OH]D), with further hydroxylation in the kidneys to its active form, 1,25-dihydroxyvitamin D, the form that acts as a steroid. In this form it suppresses prostaglandin action; inhibits p38 stress kinase signaling, tumor angiogenesis, invasion and metastasis; and inhibits NF-κB signaling.43,44
Many studies have seen a correlation between low serum concentrations of 25(OH)D and mood disorders.45 While the exact mechanisms of action haven’t been fully elucidated, vitamin D supplementation has been shown to improve mood in both depression and SAD.46,47 It should be noted that “optimal” serum levels of 25(OH)D are around 40 ng/mL.48,49
Magnesium insufficiency and frank deficiency are rampant in the US and most industrialized nations. More than half of the populous (ages ≥ 4 years) is considered to be under consuming this vital mineral.50 Chronic diseases, medications, decreases in food crop magnesium content, and the availability of refined and processed foods51 have all contributed to this epidemic.
Magnesium is the second most abundant cation in soft tissues (behind potassium) and is a cofactor for more than 300 enzymes. It plays a role in adenosine triphosphate (ATP) production, neuronal activity, cardiac function, electrical properties of cell membranes, has antispasmodic effects, and assists in glutathione synthesis.52,53 In addition to all of these accolades, it has anxiolytic properties, increases stress tolerance, and is a great antidepressant.54-56 The recommended daily allowance (RDA) varies by age and gender, ranging from 360 to 420 mg of elemental magnesium daily.
Zinc, well known for its immune properties, also plays an important role for mood, as it is essential for over 300 enzyme-dependent reactions.57 The RDA for males 19 years and older is 11 mg daily and for females, 8 mg daily. Therapeutically, trials have shown efficacy at much higher doses, although this depends on the condition being addressed. In many of the depression trials, a dose of 25 mg daily of elemental zinc was utilized.58,59 Excessive zinc intake can have toxic effects, as well as deplete copper, so the US Food and Nutrition Board has set the tolerable upper limit for those 19 years or older at 40 mg/day.60
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are well known for anti-inflammatory affects61,62 via suppression of NF-κB, cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β. They also have a solid reputation for assisting those afflicted with mood disorders. Doses of 500 mg to 10 grams of EPA and DHA, with many trials using 1 to 2 grams daily, have been shown to be effective in prevention and treatment of depressive disorders,63-65 with EPA having better data for efficacy than DHA.66 In bipolar disorders, there is strong evidence that omega-3 fatty acids are helpful in depression but not for attenuating mania.67
SAMe is produced in vivo from homocysteine and 5-MTHF, and also is available as a supplement. It is the body’s major methyl-group donor and is vital for membrane function and neurotransmission.68 In divided doses totaling 800 to 1600 mg daily, SAMe has been shown to be just as effective as tricyclic antidepressants with a lower side effect profile.69 It also has been shown to have a beneficial effect in depressed individuals where medication was not fully resolving their symptoms.70 It should be used with caution in bipolar disorder, as it can trigger mania.71
5-Hydroxytryptophan (HTP) is the rate-limiting intermediary in the synthesis of serotonin from L-tryptophan. The dosage of 5-HTP depends on condition, ranging from 50 mg to 3 grams daily in short studies.72-75 Commonly, it is dosed at 50 to 100 mg, one to three times daily, with some of the best evidence at this dose seen in anxiety.76,77 For depression, clinical trials have used 400-900 mg per day in divided doses.78-80 Caution is advised for those on selective serotonin reuptake inhibitors (SSRIs).
N-Acetyl-L-cysteine (NAC) a derivative of L-cysteine, but more stable,81 is well known for its function as an antioxidant and precursor to glutathione,82 acts as a mucolytic,83 has anti-inflammatory properties84 and is the treatment of choice for acetaminophen-induced hepatic necrosis.85 At 1000 mg, two to three times daily, this sulfhydryl molecule also possesses efficacy in numerous neuropsychiatric conditions.86-88 It appears to increase the uptake of cysteine, which activates a reverse transport of glutamate into the extracellular space. Restoring glutamate to the extracellular space inhibits more glutamate release, thereby improving compulsive behaviors.89
Taurine can be synthesized in vivo from cysteine. It stabilizes cell membranes, is an osmoregulator, assists in bile acid conjugation, contributes to cardiac contractility, inhibits platelet aggregation, is an antiarrhythmic and anticonvulsant, and last but not least, also functions as a neurotransmitter.90,91 Albeit, direct clinical trials of taurine on mood disorders may not exist, it has been shown to inhibit the release of excitatory neurons, like glutamate, act as a GABA agonist, inhibit TNF-α, and increase ATP production.92,93
Hypericum perforatum (St. John’s wort) is a highly revered botanical medicine with antibacterial, antiviral, anticancer (in vitro), antioxidant, neuroprotective, anti-inflammatory, and vulnerary (wound healing) properties.94 It is probably most well-known for its antidepressant effects, showing equal efficacy to tricyclic antidepressants and SSRIs, but with higher tolerability.95-97 The constituents hyperforin and adhyperforin appear to modulate the effects of serotonin, dopamine, and norepinephrine, as well as inhibit reuptake of these neurotransmitters. Most studies in individuals with depression, anxiety, and SAD show improvement with 300 mg, three times daily.98,99 Caution should be used in those on medications that interact with cytochrome P450 (CYP1A2, 2C9, 2C19, & 3A4) inducers, monoamine oxidase inhibitors (MAOIs), P-glycoprotein inducers, photosensitizers, and serotonergic agents.100
What doesn’t Curcuma longa (turmeric) do? Its virtues are endless, but one may not be aware of its efficacy in depressive disorders. Studies have shown that just 1000 mg of the herb daily is as effective as 20 mg of fluoxetine; and when used in combination with the medication, response rates for those with major depression rose from 65% to 78%.101 A 2017 meta-analysis showed again, its efficacy in depression.102 It also has been shown to reduce anxiety.103 It is postulated that it inhibits the activity of both monoamine oxidase (MAO)-A and MAO-B, increases the levels of neurotrophic factors (particularly brain derived neurotrophic factor [BDNF]), and modulates the serotonin and dopamine neurotransmission in the brain.104
Rhodiola rosea (rhodiola) is a wonderful plant that thrives in cold regions and high altitudes and is notorious for its ability to increase resistance to physical, chemical, and biological stressors.105 In vitro and animal studies have shown the constituents rhodioloside, salidroside, and tyrosol regulate the activity of serotonin, dopamine, and norepinephrine, as well as inhibit MAO-A.106-108 In depressed individuals, 340 mg one to two times daily has been shown to decrease overall depressive symptoms, emotional instability, insomnia, and somatization.109,110 Typically, dosages range from 200-600 mg daily, depending on the percentage of active constituents. Caution should be used in those with bipolar disorder, who are prone to manic episodes when given antidepressants or stimulants.111
Crocus sativus (saffron) is a well-known, brilliant yellow-red, precious spice that mostly grows in Iran, Greece, Morocco, and India, and is one of the most expensive botanicals in the world.112 It has a long history of traditional use and is considered to be an antispasmodic, thymoleptic, carminative, cognition enhancer, aphrodisiac, and emmenagogue.113 This revered spice also has been shown clinically to benefit attention-deficit/hyperactivity disorder,114 Alzheimer’s disease,115,116 anxiety117 and depression.118
It is theorized that safranal, a carotenoid found in saffron, interacts with the GABAergic system,119 modulates levels of serotonin (possibly by inhibiting reuptake),120 as well as alters levels of dopamine and norepinephrine.121 Standardized extracts containing 2% safranal, 2% crocin and small amounts of picrocrocin (% in studies unspecified), dosed at 15 mg twice daily have been shown to significantly reduce numerous parameters of depression.122-124 It is very safe and has no known drug-herb interactions.125
The use of pharmaceutical hormone replacement therapies (estrogen, progesterone and testosterone) will not be discussed in this article, but the prudent use of dehydroepiandrosterone (DHEA) and pregnenolone will be.
Pregnenolone is a ubiquitously produced endogenous neurosteroid, mostly made in the brain and adrenal glands from cholesterol. It is known as the master steroid hormone, since all steroid hormones, including cortisol, aldosterone, allopregnanolone, DHEA, progesterone, and testosterone, are made from it.126 Pregnenolone is thought to interact with the endocannabinoid (CB1) receptor, exerting antidepressant effects.127 Pregnenolone and its metabolites have also been shown to modulate GABA-A, N-methyl-D-aspartate (NMDA), cholinergic, dopaminergic, and neurotrophic systems, thus affecting neuronal excitability.128,129
In individuals with mood disorders, doses have ranged from 5 to 500 mg daily, with typical dosing of 50 to 100 mg daily. Monitoring serum pregnenolone levels every three to six months is advisable. Studies in both bipolar disorder and depression have shown significant improvements in symptoms.130,131
DHEA is the most abundant neurosteroid hormone in the human, secreted by the adrenal gland and produced in the brain.132 As a precursor to male and female sex hormones, DHEA has been shown to be effective in many health conditions; but germane to this paper, doses of 30 to 500 mg daily have been shown to be helpful in depression and dysthymia.133,134 DHEA-S, the major circulating metabolite of DHEA, is not subject to day-to-day and diurnal changes that DHEA is.135,136 For this reason, DHEA-S should be tested prior to administering the hormone to ensure it may be of benefit, as well as monitored every three to six months. Excessive administration of DHEA can cause acne and hirsutism; and as a precursor to estrogen and testosterone, there is a theoretical risk that long-term use could lead to hormone-sensitive cancers, especially if DHEA-S becomes elevated.
The aforementioned text is not an exhaustive list of safe and effective interventions to mood disorders, but rather a consolidation of what has better evidence clinically, both from published human studies and this author’s personal experience. As with any health condition, individuals should not self-treat, but rather seek out a qualified healthcare professional to discuss their health concerns and options.
By Todd A. Born, ND, CNS
Many factors over the course of a lifetime can influence your breast cancer risk. You can’t change some factors, such as getting older or your family history, but you can help lower your risk of breast cancer by taking care of your health in the following ways—
Staying healthy throughout your life will lower your risk of developing cancer, and improve your chances of surviving cancer if it occurs.
Studies have shown that your risk for breast cancer is due to a combination of factors. The main factors that influence your risk include being a woman and getting older. Most breast cancers are found in women who are 50 years old or older.
Some women will get breast cancer even without any other risk factors that they know of. Having a risk factor does not mean you will get the disease, and not all risk factors have the same effect. Most women have some risk factors, but most women do not get breast cancer. If you have breast cancer risk factors, talk with your doctor about ways you can lower your risk and about screening for breast cancer.
Research suggests that other factors such as smoking, being exposed to chemicals that can cause cancer, and changes in other hormones due to night shift working also may increase breast cancer risk.
Build brains
Docosahexaenoic acid (DHA). The brain’s nerve-cell membranes are made of fat. Ingesting a healthy fat—DHA—can help make these membranes lithe and limber enough to successfully fire off neurotransmitters and keep kids’ wits about them. “Attention, focus, processing efficiency, memory—all those are dependent on cells working effectively, and DHA will help,” says Randall Neustaedter, a doctor of Oriental medicine and author of The Holistic Baby Guide (New Harbinger, 2010). A recent study found that 4-year-olds who took 400 mg a day of DHA for four months improved their listening-comprehension and vocabulary-acquisition skills.
Because finding an effective dose of pure DHA (at least 300 mg a day) can be difficult, Robert Rountree, MD, coauthor of Smart Medicine for a Healthier Child (Avery, 1994), recommends liquid fish oil, in a child’s dose of 800 to 1,500 mg daily at a ratio of 60 percent eicosapentaenoic acid (EPA) to 40 percent DHA. In addition to brain-boosting DHA, the EPA in fish and other oils also offers a health bonus. “Anti-inflammatory EPA can help allergies and inflammation from colds and other viral things kids get,” says Neustaedter.
Algae can work as a vegetarian substitute for fish oil, says Neustaedter, but it contains only DHA, not EPA. Another vegetarian option, echium oil, converts to EPA at a 1-to-1 level, but does not convert to DHA. Flaxseed oil is mostly alpha-linolenic acid (ALA), which converts to DHA and EPA at only a 3 percent to 7 percent rate.
PS is found in foods such as eggs and soy, but only in small amounts. Thus, dietary supplements are more effective options to top off the body’s supply of PS. Neustaedter recommends 100 mg a day for children who need a brain booster. Formerly, PS supplements were derived from bovine brains, but due to concerns about mad cow disease, they are now made from soy.
Improve immunity
Vitamin D. “My top immune-supplement choice for most every child is vitamin D,” says Rountree. Vitamin D is crucial for triggering the immune system to react and fight off infections. Case in point: An April study in the American Journal of Clinical Nutrition found that daily supplements of vitamin D3 reduced the incidence of seasonal flu in schoolchildren by more than 40 percent.
In a perfect world, children would produce adequate amounts of vitamin D when they expose their skin to the sun. But most kids live far from the equator and use sunscreen, so they have fewer opportunities to catch rays. Neustaedter recommends school-aged children supplement with 2,000 IU of vitamin D3 a day. Unlike D2, D3 is natural and nontoxic, Neustaedter says.
Probiotics. These “friendly” bacteria help reestablish beneficial intestinal flora, which not only help digestion but boost immunity. “Eighty percent of the immune system is produced in the small intestine,” says Neustaedter. “Having a healthy small intestine will lead to a healthy immune system. Probiotics will go a long way to doing that.” Recent studies show that probiotic supplements may reduce the incidence of fevers, coughs, runny noses and other infections in young children.
Rountree recommends children take a mixture of Lactobacilli and Bifidobacteria—at least 15 billion colony-forming units a day.
Neustaedter says children can take elderberry extracts according to label instructions for acute sickness during the cold-and-flu season.
Soothe stress
Magnesium. “If kids have a hard time turning their minds off and going to sleep, calcium and magnesium will help,” Neustaedter says. As a calming mineral, magnesium trumps calcium, but “kids tend to need more calcium for their bones, so the two nutrients are usually given together,” says Rountree, who recommends children take 100 to 300 mg of magnesium daily, depending on their age and weight.
Lemon balm (Melissa officinalis). To soothe anxiety, Rountree points to lemon balm, “which is very safe and gentle but effective.” Researchers have found that lemon balm, in combination with other herbs—for example, valerian—may ease restlessness, anxiety and sleep disorders. Kids can drink 1 to 2 cups of freshly brewed tea daily. Or a tastier and more convenient option: glycerites, which are tinctures that use glycerin to extract the constituents from an herb rather than alcohol.
Turmeric, the warm, earthy spice, is extracted from the dried rhizome, or root, of the Curcuma longa plant. For centuries, turmeric has been used throughout India and across many parts of Southeast Asia as a spice, a preservative, a multi-purpose folk remedy, and even as a saffron-hued fabric dye. Curcumin is one of three micronutrient compounds found in turmeric—aptly named curcuminoids—that give the spice both its distinctive golden color and its healthy benefits. Surprisingly, curcumin only makes up a mere 2–5% of most dietary preparations of turmeric.
While curcumin has been used as a folk remedy since ancient times, it wasn’t formally studied until the 21st century, but it’s certainly making up for lost time. Since the first scientific article on curcumin was published back in 1937, over 2,600 research studies have been published in English language journals. Curcumin has been extensively researched for a wide variety of potential health benefits, with a majority of studies exploring its powerful anti-oxidative properties, as well as its role in supporting a positive response to inflammation at the cellular level.*
As a potent natural antioxidant, curcumin helps support cells facing the damaging effects of free radicals.* Curcumin influences a variety of cell signal pathways and helps reduce systemic oxidative stress in cells, organs, and tissues throughout the body.* Using several different mechanisms, curcumin helps neutralize free radicals by scavenging reactive oxygen, nitrogen, and peroxyl radicals, as well as modulating enzyme activity. By helping to reduce oxidative stress, curcumin helps benefit our cells by supporting their structural integrity and maintaining healthy function.*
Curcumin has also been praised for its ability to naturally promote a healthy response to inflammation.* While this all sounds great, what does it really mean? For starters, let’s remember that not all inflammation is bad. Temporary inflammation is a normal, healthy defense mechanism used by the body to facilitate healing following an acute injury, infection, or allergic reaction. Scabbing, redness, and swelling are all indicators of normal, acute inflammation. For many people, poor diet can hinder the body’s ability to resolve inflammation in a timely way. When this occurs, it may be beneficial to supplement with curcumin which influences pathways related to the body’s immune response and can help facilitate an optimal response to inflammation.*
In its native form, curcumin is not especially water soluble, and therefore very difficult for the body to absorb and use. In technical terms, it suffers from poor bioavailability.
When curcumin enters the body’s digestive tract, its chemical structure makes it prone to picking up a sugar molecule, which renders it essentially inactive and puts it on the fast-track for excretion before it can be absorbed and circulated throughout the body. Unfortunately, this means no matter how many delicious bowls of yellow curry you enjoy, your body probably isn’t getting enough curcumin to significantly feel its health benefits.
Many creative methods have been tried to address curcumin’s inadequate native bioavailability. Some curcumin supplement products add black pepper extract—also known as piperine—to improve absorption by preventing those pesky sugar molecules from latching onto curcumin. However, this approach is less than ideal since piperine might also affect the metabolism of substances besides curcumin—including prescription drugs.
You don’t have to be a doctor to know that proper dosage of medication is very important. Since doctors prescribe pharmaceutical dosages assuming a certain level of bioavailability, changing the body’s ability to metabolize prescription drugs could be problematic. All things considered, you could argue that using piperine simply isn’t worth the risk.
Nordic Naturals’ new Curcumin Gummies and synergistic formulas that feature curcumin like Omega Curcumin use a specially developed type of curcumin—Longvida® Optimized Curcumin—which is made using a proprietary process called Solid Lipid Curcumin Particle Technology (SLCP™) developed at UCLA. By surrounding natural curcumin in a liposome (a ball of fat-like molecules), Longvida Optimized Curcumin protects the micronutrient and helps it move across the gut wall and into the bloodstream where it can be circulated and absorbed throughout the body.
Thanks to SLCP™ technology, Nordic Naturals’ curcumin products are 65 times better absorbed than standard curcumin products that claim 95% absorbability using the C-Max method, which measures absorbability at a single point in time. Using the Area Under the Curve (AUC) normalized method, which measures absorbability over time, Nordic Naturals’ curcumin products boast 285 times better absorbability. No matter which method is used, it’s clear that Longvida Optimized Curcumin offers absorption and benefits that other forms of curcumin can’t.
For centuries, turmeric’s unique, earthy flavor has been reason enough for countless people to use it as a cooking ingredient on a regular basis. Since then, we’ve learned the powerful micronutrient curcumin is the reason behind turmeric’s therapeutic properties as well as its signature golden color. Since the body can’t efficiently absorb curcumin in its native form, adding a bioavailable curcumin supplement is a smart and healthy way to spice up your daily health routine.
BY ROB HUGHES
PRODUCTS TO TRY:
Fish oil or krill oil; that is the omega-3 question of the decade. Fish oil certainly has a long history with a plethora of research to validate its health benefits, but suddenly krill oil moves into the neighborhood making claims of superiority and seeming ready to displace the position fish oil has occupied for so long. Many of us consciously or subconsciously operate under the idea that newer is better, which may cause us to side with krill oil, but this philosophy doesn’t always hold water. Maybe the question is not an either/or scenario, but rather, what are the strengths and limitations of each that may warrant the use of both.
The Argument
The argument for choosing either fish oil or krill oil is rooted in studies that suggest krill oil may be more effective at building tissue levels of omega-3 polyunsaturated fatty acids (n-3 PUFA). This conclusion stems from the fact that up to 65 percent of the omega-3 PUFAs in krill oil are esterified as phospholipids (PL) rather than triacylglycerols (TAG), which are the exclusive form found in fish oil. Phospholipids are generally considered to have a higher bioavailability, being the main component of cell membranes, and are more efficiently absorbed by brain tissue, especially.
The Truth About Bioavailability
Even though logic suggests the bioavailability of phospholipid-based omega-3 PUFAs is better than the traditional TAG form, the proof is always in the studies.
This logic was put to the test in an animal study and the results were published earlier this year (2019). Mice were fed either a control diet or one of six DHA (1%, 2%, or 4%) as PL-DHA or TAG-DHA diets for 4 weeks. Both the PL-DHA and TAG-DHA diets resulted in higher DHA concentration in liver, adipose, heart, and eye, but not brain tissue. However, there was no significant difference in DHA concentration in all tissues between the PL- or TAG-DHA forms. Additionally, all tissue types showed higher levels of EPA PUFAs for both PL-DHA and TAG-DHA diets. According to this study, the PL form of omega-3 PUFAs doesn’t seem to increase DHA and EPA any more significantly than the TAG form.
In another animal study, published in 2018, researchers investigated the effect of oral short-term and long-term administration of krill oil and fish oil on bioavailability in the blood and brain of rats. Rats were given 1000mg of either fish oil, krill oil made by enzyme extraction, krill oil made by solvent extraction, or control. Blood and brain samples were collected after 2, 4, 8, 12, 24, 48 h of oral administration. Rats were then given 500mg daily for 2 weeks of the same test oils or control and then blood and brain samples collected for long-term evaluation. Results showed that PUFA content in the brain was higher in the short-term among rats receiving krill oils. In the long-term, there was a slightly greater level of EPA and DHA in the brains of rats receiving krill oils compared to fish oil, but the difference was not significant. In the long-term, there was no significant difference between blood levels of DHA among rats receiving either krill or fish oils, but those receiving fish oil did show slightly higher blood concentrations of EPA.
Other Metabolic Markers
What about the effects of krill oil or fish oil on metabolic markers such as fasting serum TAG levels, total lipids, phospholipids, cholesterol, cholesteryl esters, non-esterified cholesterol, vitamin D, and fasting glucose? According to an 8-week randomized parallel study of thirty-six healthy subjects aged 18 to 70 years receiving either fish, krill oil or control oil, fasting serum TAG did not change between the groups, blood glucose decreased significantly in the krill group, vitamin D increased significantly in the fish group, and all other markers increased significantly in the krill oil group.
The Benefits of Krill Oil
Krill is distinct from fish oil not only because of its higher phospholipid content, but also because it contains a unique antioxidant profile which includes the powerful antioxidant, astaxanthin. Astaxanthin has been shown to impart significant health benefits on eyes and skin, but also possesses anticancer, antidiabetic, anti-inflammatory, and antioxidant activities. Krill oil also offers a more sustainable form of PUFAs, coming from a large stock of Antarctic crustaceans with a much higher reproduction rate compared to cold-water fish.
The Benefits of Fish Oil
Fish oil still boasts of significantly higher levels of both EPA and DHA, compared to krill oil and although advocates of krill oil argue that bioavailability is better, studies aren’t showing a significant difference, meaning fish oil may still be a superior means of raising the concentrations of these PUFAs. Fish oil can also be easily obtained in clinically relevant doses by consuming cold-water fish. In this way, consumers are also reaping the benefits of other nutrients found in fish including iodine, selenium, taurine, high-quality proteins, and vitamins D and B12. And due to its wide availability, fish oil remains more cost-effective.
Despite being apparent rivals, krill and fish oil may not be mutually exclusive after all. Instead, each may play a role the other cannot fulfill, making their combined use beneficial and even preferred.
By William Faloon
Predicting which nutrients will emerge as life-saving superstars can be challenging.
For example, a vitamin introduced just a decade ago is demonstrating profound anti-aging effects that extend far beyond its original indications.
Based on an abundance of positive findings, scientists have developed a more cost-effective form of this nutrient that enables it to stay in the body much longer than before.
The incredible news is that maintaining constant levels of this nutrient not only protects against atherosclerosis, but may reverse arterial calcification as well!
A wealth of studies published in 2008 reveals this same nutrient possesses anticancer properties while suppressing factors involved in common age-related diseases.1-15
A hallmark of normal aging involves calcification in soft tissues throughout the body such as heart valves, glands, and blood vessels.16-18
One might erroneously think that dietary calcium is a culprit behind pathological calcification processes. The opposite is true. When rabbits are fed calcium-deficient diets, calcification rates rise by 2.7-fold. Calcium-supplemented diets, on the other hand, reduce calcification by 62%.19
The reason for this contradiction is that in response to a deficit of calcium in the blood, the body excessively robs our bones20 and saturates soft tissues with calcium.
As we age, we lose our ability to regulate calcium balance and then suffer the lethal consequences of systemic calcification. It is encouraging to know that a low-cost nutrient (vitamin K) can quickly restore calcium homeostasis.
Warfarin (Coumadin®) is an anticoagulant drug that inhibits normal vitamin K function in the body. The alarming result of vitamin K impairment is rapid development of osteoporosis and arterial calcification.21,22
Vitamin K is absolutely essential for regulating calcium balance in the body. A deficiency of vitamin K status causes brittle bones and a vascular system that hardens to a state of poor functionality.23-26
People who take Coumadin® suffer more osteoporotic fractures21 and show substantially more abnormal calcium deposition in other areas, such as heart valves—twice as much as non-Coumadin® takers.22
The fact that these pathological changes are allowed to occur in humans prescribed warfarin is unconscionable given the knowledge about the value of low-dose vitamin K supplementation, even in patients at high risk for abnormal arterial blood clots.
Atherosclerosis is the leading cause of disability and death in civilized societies. Many factors are involved in its initiation and progression.27,28 Homocysteine or oxidized low-density lipoprotein (LDL) can initially damage the inner arterial lining (the endothelium).29 To repair this damage, the endothelium produces collagen that forms a cap over the injury site.
These endothelial collagen caps attract calcium that accumulates (calcifies) and forms a hard material resembling bone. This is why atherosclerosis is sometimes referred to as “hardening of the arteries.”
Calcification of the coronary arteries markedly increases heart attack risk.30
A substantial volume of studies shows that insufficient vitamin K2 accelerates arterial calcification.31 A new study shows that restoring vitamin K2 reverses arterial calcification.49
Vitamin K functions to keep calcium in the bone and prevent its buildup in the arteries.23-26,28,31 If that is all vitamin K did, it would be one of the most important nutrients for aging humans to take. Newly published research, however, indicates vitamin K2 possesses a host of additional benefits.
Bone is living tissue that is in a constant state of renewal. The maintenance of bone first requires old bone to be dissolved by cells called “osteoclasts.” When the activity of osteoclasts is too high, large holes develop that weaken the bone and lead to osteoporosis. Vitamin K2 is a key to turning off excess osteoclast activity and bone degradation.
The holes left by osteoclasts are prepared for remodeling by osteoblast cells. The osteoblasts secrete a protein called osteocalcin, which when activated (or carboxylated) enables new calcium to be laid down into the bone. The calcium-binding properties of osteocalcin require vitamin K, whereas the synthesis of osteocalcin itself requires vitamin D3.
Vitamin K thus provides two critical benefits to the bone. It first protects against excess bone degradation (resorption) by turning off excess osteoclast activity. It then supports the critical role of new bone formation by enabling osteocalcin to pull calcium from the blood and layer it on to the bone.
From this brief description, it is clear that maintenance of healthy bone density requires adequate levels of calcium, vitamin D, and vitamin K. Without vitamin D, there will be no osteocalcin for vitamin K to work on. Without vitamin K, the osteocalcin that is produced will be inactive. And of course without calcium (and other minerals), there will be no minerals for the activated osteocalcin to attract to the bone for structural density.
The Nurses’ Health Study followed more than 72,000 women for 10 years and found that women whose vitamin K intakes were in the lowest quintile (1/5) had a 30% higher risk of hip fracture than women with vitamin K intakes in the highest four quintiles.67
A seven-year study in over 888 elderly men and women (Framingham Heart Study) found that men and women with dietary vitamin K intakes in the highest quartile (1/4) had a 65% lower risk of hip fracture than those with dietary vitamin K intakes in the lowest quartile (approximately 254 micrograms/day vs. 56 micrograms/day of vitamin K).68
Vitamin K2 has proven to be as effective as prescription drugs in reducing the incidence of bone fractures. A Japanese study in postmenopausal women compared the effect of K2 (MK-4) with the drug etidronate (Didronel®) on the incidence of vertebral (spine) fracture. Women taking K2 at a dose of 45 mg per day experienced a fracture rate of 8.0% compared with 8.7% for those taking the etidronate drug therapy. Furthermore, women taking both MK-4 and the drug experienced only a 3.8% fracture rate. In a placebo group that received neither K2 nor drug therapy, nearly 21% of women experienced bone fractures.69
Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation in the joints and other organs in the body. Those afflicted with rheumatoid arthritis have startlingly high rates of cardiovascular diseases.33
In a study published in June 2008, Japanese scientists found that vitamin K2 inhibited the proliferation of synovial cells and prevented the development of collagen-induced rheumatoid arthritis in the rat model. The scientists concluded that vitamin K2 may represent a new agent for the treatment of rheumatoid arthritis in combination with other anti-inflammatory drugs.34
A recent human study showed that the use of vitamin K2 alone or in combination with bisphosphonate drugs (like Fosamax®) for treatment of osteoporosis in patients with rheumatoid arthritis may inhibit osteoclast induction via decreases in levels of inflammatory mediators.35 Excess osteoclast activity depletes bone mineral density.
Americans afflicted with osteoporosis or low bone mineral density scores are sometimes prescribed drugs like Fosamax® or Actonel®. Side effects from these drugs sometimes preclude their long-term use.
Japanese patients are often prescribed high doses of vitamin K2 instead of drugs. Published studies demonstrate the ability of vitamin K2 by itself to halt the loss of bone mineral density.23,36,37
A study published in May 2008 used both Fosamax® and vitamin K2 in postmenopausal women in Japan for one year. The results showed that addition of vitamin K2 led to a greater increase of femoral neck bone density, compared with Fosamax® alone. The doctors confirmed the specific bone-protecting mechanism unique to vitamin K2, a finding that had been established in previous studies.38
Doctors in Germany conducted a study examining the relationships between dietary intake of vitamin K1 and K2 on the development of prostate cancer in 11,319 men over an 8.6-year follow-up.4
Compared with the lowest intake of vitamin K2, men with the highest vitamin K2 dietary consumption showed a 63% reduced incidence of advanced prostate cancer. Intake of vitamin K1 was not related to prostate cancer incidence in this 2008 study.4
Skeletal fractures cause significant disability and there is growing interest in identifying methods to accelerate the healing time of broken bones.
The synergistic effect of vitamin D3 and vitamin K2 in preventing osteoporosis has been documented in clinical practice.39 Up until now, however, there were no reports investigating if these nutrients could enhance fracture healing.
An in vitro study published in January 2008 showed that combining vitamins D3 and K1 favorably modulated the proliferation and differentiation of cells required to heal bone. This led the doctors to conclude that these nutrients taken together offer clinicians a promising low-cost strategy for laying down new bone material.39
Vitamin K2 induces differentiation and apoptosis in a wide array of human cancer cell lines. A search of PubMed reveals studies published in 2008 that discuss the role of different forms of vitamin K in the treatment of cancer.1-15
A goal of cancer researchers is to identify compounds that cause cancer cells to self-destruct. Vitamin K2 has been shown to induce apoptosis (cell destruction) in leukemiacells in vitro. A study published in July 2008 identified yet another pathway by which vitamin K2 causes the degradation (via autophagy) of leukemia cells’ own components. The scientists noted that apoptosis and autophagy in leukemia cells could be simultaneously induced by vitamin K2.8In the laboratory, vitamin K2 demonstrates inhibitory effects against myeloma and lymphoma, suggesting possible applications for individuals fighting these all too common cancers.40
Infection with the hepatitis B or C virus is a major risk factor in developing primary liver cancer, known medically as hepatocellular carcinoma. It can also occur in those who do not have hepatitis. A study published in the Journal of the American Medical Associationshowed that in those with viral-induced liver cirrhosis, less than 10% of patients given vitamin K2 developed liver cancer. In similar patients not given vitamin K2, a startling 47% developed primary liver cancer.41 Vitamin K2 decreased the risk of hepatocellular carcinoma to about 20% compared with the control group.
In a study published in early 2008, 61 primary liver cancer patients who were in remission after treatment were separated into two groups. One group was given supplemental vitamin K2. After one year, only 13% of the group that received K2 experienced recurrence of liver cancer, compared with 55% of the group who did not receive K2. Three-year survival in the vitamin K2-supplemented group was 87% compared with 64% in the group not receiving the vitamin K2.42
In 2007, scientists identified specific anticancer mechanisms for vitamin K2, including inhibition of proinflammatory nuclear factor-kappa B (NFkB) that is often over-expressed in cancer cells.43 Tumor cells use proinflammatory factors to develop survival mechanisms that thwart conventional attempts to eradicate them.
Drugs like Coumadin® that antagonize vitamin K do more than cause bone loss and arterial calcification. In a model of melanoma in mice, the oral administration of anticoagulant drugs that antagonize vitamin K “drastically promoted metastasis.” The promotion of metastasis was almost completely suppressed by the pre-administration of vitamin K3, suggesting that these anticoagulant drugs promote metastasis by specifically antagonizing vitamin K.44
While vitamins K1 and K2 are safe and effective, vitamin K3 is potentially toxic and its use has been limited to treating aggressive cancers. A study published in early 2008 identified several specific mechanisms by which vitamin K3 damages pancreatic cancer cells, leading the researchers to state that, “the action of vitamin K3 may lead to a favorable outcome against pancreatic cancer.”7
Apatone® is a drug consisting of vitamin C and vitamin K3. It has been granted orphan drug status by the FDA to treat advanced bladder cancer.
Apatone® selectively targets tumors by entering cancer cells as readily as glucose. It then suppresses inflammatory responses (such as those induced by nuclear factor-kappa B) that cancer cells use to escape destruction by chemotherapy agents. Vitamin K3 is being clinically tested as an agent to administer prior to chemotherapy to decrease the resistance tumor cells develop to chemo drugs.
In March 2008, the results of a study were published on prostate cancer patients who had failed standard therapy and were given the drug Apatone® at a dose that equaled 5,000 mg of vitamin C and 50 mg of vitamin K3. The results showed that PSA velocity decreased and the time it took PSA to double increased in 13 of 17 patients. Of the 15 patients who continued on Apatone®, only one death occurred after 14 months of treatment. The doctors concluded, “Apatone® showed promise in delaying biochemical progression in this group of end stage prostate cancer patients.”5
Based on the plethora of studies published in 2008, vitamins K2 and K3 have emerged as intriguing agents in both cancer prevention and treatment.
Normal deposition of calcium occurs in only two places: bone and teeth.
Abnormal (pathological) deposition of calcium occurs in multiple tissues including:
Vitamin K2 appears to be the most important factor in steering calcium into the bone and away from heart valves and the arterial system.
While vitamin K is required for healthy blood clotting, taking too much does not increase the risk of an abnormal clot. The reason is that vitamin K causes a complete chemical conversion (carboxylation) of coagulation-dependent proteins in the body to put them into an active form.
Once these coagulation proteins are acted upon by vitamin K, they are 100% carboxylated. If you take additional vitamin K, nothing will happen because all of the coagulation proteins that can be carboxylated are already carboxylated. It is not possible to over-carboxylate coagulation proteins because they are already 100% carboxylated by the vitamin K you took.
Patients predisposed to abnormal blood clots, such as those with mechanical heart valves, atrial fibrillation, or prothrombotic factors in the blood are prescribed drugs like warfarin that interfere with the carboxylation of coagulation proteins. It is only in patients taking these anticoagulant drugs that the dose of vitamin K and the drugs need to be closely measured to achieve the optimal therapeutic INR range (usually around 2.5 in people who take warfarin).
To demonstrate the safety of vitamin K2, people living in the Japanese regions where natto is regularly eaten have several-fold greater blood levels of vitamin K2 (MK-7).36 The effect of high amounts of vitamin K in the blood is less osteoporosis, fewer bone fractures, and fewer heart attacks.23,30,36,46,63-65
As we age, calcium deposits tend to accumulate in soft tissues throughout our bodies.
Doctors performing autopsies on elderly people used to comment that it appeared that the soft tissues in these once supple bodies had turned to stone. These doctors were referring to the systemic calcification occurring virtually everywhere except the skeleton.
Systemic calcification means that calcium that is supposed to be deposited in the bones is instead being lodged in soft tissues where it does not belong. Many age-related diseases can be linked to calcification including kidney stones, arthritis, cataracts, heart valve insufficiency, bone fractures, wrinkled skin, bone spurs, senility and, of course, coronary atherosclerosis. Restoring optimal vitamin K status may help to protect against all of these disorders.
Osteoporosis is a classic age-related disease. A systemic review of 13 randomized controlled human trials that gave adults either vitamin K1 or K2 supplements for at least six months found that except for one, supplemental vitamin K1 or K2 reduced bone mass loss. Vitamin K2 in particular was associated with increased bone mineral density.66
In all trials to evaluate fracture risk, vitamin K2 was most effective. It reduced the risk of vertebral fractures by 60%, hip fractures by 77%, and all non-vertebral fractures by an astounding 81%.66
As can be seen on the chart on this page, higher ingestion of vitamin K results in a 26% reduction in all-cause mortality.46
Based on the enormity of published scientific studies, maintaining optimal vitamin K status would appear to be an essential component of a comprehensive anti-aging program.
Seasonal allergies are not only culprits that keep people from enjoying the bloom of spring or the coolness of fall, but they can be painful and miserable altogether, sometimes even triggering mood disorders. The pollen and mold trigger a rise in proinflammatory leukotrienes and prostanoids in the mucus membranes, and ushers in an army of mast cells and eosinophils. These players begin battle by degranulation and cytokine release, which calls for more reinforcements. Clinically, the host of this battle experiences a runny, itchy nose, sneezing, watery eyes, congestion, fatigue, and sometimes a mild fever.
Nettle Leaf (Urtica dioica)
Nettle, also known as stinging nettle, is commonly known for its efficacy in managing symptoms of seasonal allergies. However, this plant is also surrounded by irony since touching its leaves often results in allergic dermatitis that leaves its victim itching and red. The extract of nettle contains compounds identified as antagonists to the Histamine-1 (H(1)) receptor while also inhibiting mast cell tryptase and preventing the degranulation and release of a host of pro-inflammatory mediators that cause the symptoms of seasonal allergies. Further, nettle extract targets the inflammatory pathways by inhibiting cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and hematopoietic prostaglandin D(2) synthase (HPGDS), all of which are central enzymes in proinflammatory pathways and contribute to prostaglandin production. Clinically, these actions help to decrease allergic rhinitis – one of the most common (and albeit, annoying) symptoms of allergies.
To discover the tangible benefits of nettle extract in managing allergic rhinitis, a randomized, double-blind, placebo- controlled, clinical trial was conducted on 40 patients, assigned either 150mg of Urtica dioica or placebo for one month. Results showed a significant improvement in the severity of allergic rhinitis in both groups; however, those taking nettle had lower eosinophil counts on a nasal smear, compared to placebo. Although this study should be followed up by a more robust study, it suggests nettle can be useful in mitigating the immune responses that trigger common symptoms of seasonal allergies, such as allergic rhinitis.
Guduchi (Tinospora cordifolia)
A less well-known botanical that is immensely useful in managing the symptoms associated with seasonal allergies is Tinospora cordifolia, also known as Guduchi. Commonly used in Ayurvedic medicine, this plant possesses an impressive array of therapeutic properties including anti-diabetic, anti-periodic, anti-spasmodic, anti-inflammatory, anti-arthritic, anti-oxidant, anti-allergic, anti-microbial, anti-osteoporotic, anti-stress, anti-leprotic, anti-malarial, hepatoprotective, immunomodulatory and anti-neoplastic activities. These activities are possible because of the variety of biological compounds including alkaloids, diterpenoid lactones, glycosides, steroids, sesquiterpenoid, phenolics, aliphatic compounds, and polysaccharides.
A highly activated immune response is responsible for most of the symptoms associated with seasonal allergies and many of the compounds found in Guduchi have immunomodulatory effects. More specifically, they have been reported to boost the phagocytic activity of macrophages, influence cytokine production, and activate immune effector cells, enhancing the immune response.
So how does this seemingly amazing botanical function in studies of seasonal allergy symptoms? In a randomized double blind placebo controlled trial, seventy-five patients were given either Tinospora cordifolia or placebo for 8 weeks. In the group receiving Tinospora cordifolia, there was complete relief from sneezing in 83 percent of the patients, nasal discharge in 69 percent, nasal obstruction in 61 percent, and nasal pruritis in 71 percent. In the placebo group, there was only complete relief from sneezing in 21 percent of the patients, nasal discharge in 15.2 percent, nasal obstruction in 17 percent, and nasal pruritis in 12 percent. The significant chasm between these outcomes gives impressive evidence of the usefulness of Tinospora cordifolia in managing symptoms of seasonal allergies.
Unfortunately, for some seasonal allergies seem to linger far longer than the onset of the season. Since the symptoms in seasonal allergies are rooted in the immune system, the health of the microbiome cannot be ignored when considering the balance and robustness of an immune response. Therefore, good quality probiotics and a high-protein/low-sugar diet can also help support a healthy immune response during a particularly challenging season.
According to a new study just published 3 days ago in the journal Circulation high dose fish oils post heart attack improved heart function and reduced scarring.
After a heart attack the shape and function of the heart can change which could end up leading to heart failure. Unfortunately there are limited things that can improve healing of the heart or prevent adverse remodeling. This new study demonstrates the significant role of omega-3 fatty acids in supporting the structure and tissue of the heart.
The study included 360 heart attack survivors. Researchers compared patients taking 4 grams of omega-3 fatty acids daily for six months to those taking a placebo. There was a 5.8% reduction in left ventricular end-systolic volume index (predicts patient outcome) and a 5.6% reduction in fibrosis formation in the non-damaged heart muscle of the fish oil group.
The treatment was safe and effective. Both groups received treatment based on guidelines issued by the American College of Cardiology Foundation and the American Heart Association. Blood tests were used to confirm that patients in the omega-3 fatty acids group were compliant to the treatment.
This study is significant since heart failure is a major problem post heart attack. The results demonstrate that omega-3 fatty acids help to improve cardiac remodeling which allows the heart to contract better and decreases fibrosis in the region that is not damaged.
Fish oil supplementation is essential for cardiovascular health. Some doctors recommend fish oils to improve LDL particle size and lower triglycerides as well as for their anti-inflammatory properties and simply for their support of overall health since these fats are essential for the normal function of all of our cells.
Patients with heart failure are individuals who have a disruption in their metabolic processes and as the heart muscle weakens it cannot meet metabolic demands. Thus additional nutrients are also essential for these individuals including the energy-supportive nutrients ribose CoQ10 and l-carnitine.
Ribose is a key nutrient for quickly restoring cardiac energy stores. It is needed to synthesize adenine nucleotides certain vitamins and other important cellular compounds.
CoQ10 plays a central role in the production of ATP and is required for muscle contraction and other cellular processes.
Carnitine supports the heart by the delivery of fat to the heart muscle which is its main fuel source.
In addition magnesium and potassium should be considered to support all cardiovascular conditions. These nutrients are often depleted in heart failure most commonly by the use of diuretic medications.
By Michael Jurgelewicz DC DACBN DCBCN
