Category Archives: Nutrition

Adding Bitter Flavors to Decrease Glucose intake | Medical Weight Loss Alexandria Virginia

The above is a video from Wholistic matters. There was a recent study from the AHA demonstrating that individuals with differences in the ability to taste bitter may have altered intake of vegetables, which generally have a bitter taste.

Different variants of the taste gene TAS2R38 are the source of the bitter perception. There are two primary variants : an AVI and PAV Varianta. The AVI variant does not perceive bitter taste as much and was found that individuals with this SNP consumed more vegetables.

Individuals whose genetic code is written to perceive certain plant compounds as particularly bitter are less likely to eat vegetables. This is according to data analysis from 175 submissions to a food frequency questionnaire, where researchers associated certain eating habits with different variants of the taste gene TAS2R38. This research was presented as part of the American Heart Association Scientific Sessions 2019.

Is Taste Perception Genetic?

Humans have numerous receptors in the body that are responsible for taste perception, and the TAS2R38 gene encodes a protein that controls the perception of certain bitter tasting compounds of Brassica plants, also known as cruciferous vegetables. Specifically, the TAS2R38 bitter taste receptor manages the taste of certain glucosinolates, a type of phytonutrient found in cruciferous vegetables such as broccoli, cabbage, kale, and Brussels sprouts.

Many variants of the TAS2R38 gene have been identified worldwide, but two predominant common forms exist with vastly different effects on bitter perception: “PAV” and “AVI.” An individual with two copies of the AVI variant will be less likely to perceive bitter tastes from bitter compounds, while an individual with two copies of PAV will find bitter compounds extremely bitter. Someone with one copy of each variant will perceive bitterness somewhere in the middle of the spectrum.

In the recent study, researchers found that people with two copies of the PAV gene were 2.5 times more likely to “rank in the bottom half of participants on the number of vegetables eaten,” presumably because these individuals find bitter compounds in many vegetables unpalatable and unpleasant.

Are Bitter Foods Good for You?

As explained in this animation, “Managing Glucose Response With Bitter Nutrition,” bitter compounds are important for carbohydrate processing. The small intestine is lined with both glucose transporters and bitter receptors. Carbohydrates are metabolized into glucose, which is absorbed into the blood via glucose transporters, and compounds from bitter-tasting foods bind bitter receptors to help regulate glucose transport. When the diet contains excessive glucose and insufficient bitter compounds, chronically elevated blood glucose levels can lead to chronic conditions like obesity, metabolic syndrome, and diabetes.

What Foods are Bitter Tasting?

Plant-based foods with bitter compounds include cruciferous and green leafy vegetables (broccoli, Brussels sprouts, and kale), soybeans, citrus fruit (grapefruit, orange, lemon, and lime), green tea, red wine, and oats. Plant-based foods are often perceived as bitter because they contain phytonutrients, which have bitter properties. Plants produce phytonutrients as a protective mechanism, and when humans consume them, they reap health benefits as well. Plant-based phytonutrients are associated with the prevention of chronic conditions.

What Does Processing Do to Food?

Because many people perceive bitter compounds as disagreeable, food processing removes many naturally occurring bitter compounds. In this podcast, “Phytochemicals, Bitter Receptors, and Carbohydrate Processing,” Slavko Komarnytsky, PhD, describes how food technology of the last century engaged special food processing that removes bitter compounds from food to make it more enjoyable. Consuming processed food that has been “de-bittered” prevents bitter compounds from interacting with bitter receptors in the small intestine and regulating healthy carbohydrate processing.

Historically, in the absence of refined grains and unnaturally large pieces of fruit, human intake of carbohydrates was low. But with crop domestication and agricultural techniques of the past few decades, humans have exponentially greater access to carbohydrates, and the human body struggles to manage this influx of carbohydrates.

For more on bitter compounds and modern day breeding practices that affect natural sources of bitter compounds, listen to the podcast with Eric Jackson, PhD: Oats, Bitter Compounds, and a Lifetime of Plant Study.

How Can the Study of Genetics Improve Health?

Researchers from the American Heart Association presentation hope to expand upon their current study by using genetics to predict which vegetables people will like based on their TAS2R38 profile. And for people with two copies of PAV, genetic studies could help researchers identify certain spices to improve palatability of bitter foods. The better a food tastes, the more likely the average human will eat it. The more vegetables a person eats, the better.


Eating And Lifestyle For Better Hormone Health In Peri-Menopause

While women’s hormone health is always foundational to overall wellness, a time called perimenopause—the years before menopause, when the ovaries begin to make less oestrogen—is characterized by significant hormonal shifts, in addition to negative symptoms including anxiety, depression, night sweats, and more. .By consuming larger amounts of cruciferous vegetables, which “promote estrogen metabolism and detoxification in the liver,” the article mentions incorporating flaxseed into routines, focusing on foods that support bone health, eating plenty of omega-3-rich foods, and replacing simple & processed sugars with more high-fiber complex carbohydrates. Overall, the research supports a strong focus on foods that “decrease inflammation, support a healthy mood, and balance hormones and insulin levels.”

Here at Compounding Lab , we’re all about women’s hormone health. We strongly believe that our hormones benefit from a healthy lifestyle and that every green smoothie, yoga , pilates class, and minute of meditation matters. But there’s a time in every woman’s hormonal life—called perimenopause—that’s long been overlooked. This era is marked by big hormonal shifts that can greatly affect quality of life, causing a lot of anxiety and discomfort. So this week, lets get down and dirty and uncover our hormones so that we’re all more informed and empowered.

So perimenopause refers to the years that precede menopause, when women can experience unwelcome symptoms of hormones changing like night sweats, mood swings, irritability, depression, missed or heavy periods, and vaginal dryness. These symptoms are no walk in the park! Most women start experiencing perimenopause n their mid-40s, but for some women it will begin as early as their 30s.

So what’s happening to your hormones during this time? During perimenopause, oestrogen and progesterone hormones start to decrease. Progesterone tends to drop first, and oestrogen can fluctuate up and down until it settles. You can’t avoid these hormonal changes altogether, but you can do a lot to empower yourself with specific dietary and lifestyle choices that help you feel more like yourself. Here are some important foods I tell women to focus on during this time in your life:

1. Load Up On Cuciferous Vegetables.

In the early stages of perimenopause, progesterone drops faster than oestrogen. This can lead to oestrogen dominance, or a higher oestrogen level compared to progesterone. During this phase, it’s important to support the body’s ability to metabolize oestrogen properly, and vegetables from the cruciferous family are best at that. “Rich in indole 3-carbinol and chlorophyll, these veggies promote oestrogen metabolism and detoxification in the liver, shifting ‘dirty’ oestrogens to ‘clean’ oestrogens,” I recommend eating cruciferous vegetables on a daily basis during perimenopause. If you’re not used to consuming this type of vegetable and need some inspiration, try sautéing and incorporating broccoli, Brussels sprouts, and bok choy into omelets and stir-fries. You can also mix raw shredded broccoli, cabbage, or Brussels sprouts into your salads. One of my favorite substitutes is to make cauliflower rice instead of mashed potatoes or white rice for more fiber and fewer carbs. Or, simply snack on cruciferous veggies alone or dipped in guacamole or hummus. If they cause gas or bloating, start slowly and stick with cooked forms, as cooking these cruciferous veggies makes them easier for your digestive system to tolerate. If you can’t tolerate them FIX your GUT girls.

2. Eat Protein-Rich Foods At Every Single Meal , Especially Breakfast At Around 10am

Blood sugar issues during perimenopause will worsen your mood swings, increase irritability, and stress your adrenals. Eating protein at every meal will stabilize blood sugar and reduce the spikes and crashes, which will also help you lose weight, prevent weight gain, and reduce your risk for insulin resistance, diabetes, and metabolic syndrome. Protein also helps you stay full and burn more calories without feeling deprived or constantly hungry. Your muscle mass and bone density take a hit as you enter menopause, and getting enough protein in your day, along with resistance training or weights will preserve them and reduce their decline. The best high-protein foods to incorporate into your diet are pastured eggs, wild-caught fish, lean poultry, grass-fed meats, and legumes (if you can tolerate them). Aim for 21 to 28 grams of protein at each meal, including breakfast. Skip the morning pastry and have a savory breakfast like a vegetable omelet or organic, preservative-free turkey or chicken sausage with some broccoli or cauliflower. If you like oatmeal, add high-protein nuts and seeds like almond butter, hemp, or pumpkin seeds for a delicious and high-protein treat.

3. Incorporate Flaxseed Into Your Routine.

Flaxseed can be one of the most supportive superfoods throughout perimenopause. Carper frequently recommends it in the later perimenopause stages as it contains lignans, which are phytoestrogens, weaker plant-based oestrogens that provide gentle oestrogen support when estrogen is waning. Conversely, she adds, “it can act adaptively and block oestrogen when oestrogen dominance is present in the earlier stages.” That said, if adding flaxseed worsens your periods, mood swings, breast tenderness, or other symptoms you’re experiencing, it may be amplifying your oestrogen dominance, and you should discontinue use. Expert tip: Always grind flaxseeds to reap the benefits, as we don’t have the digestive enzymes needed to break down the outer shell. If possible, buy them whole, grind them in small batches every few days, and store in the fridge to maximize freshness. Flaxseeds can be enjoyed in smoothies, as an egg replacement in vegan or egg-free recipes, or simply added to casseroles or Greek yogurt. If you’re into healthy baked goods, you can also use ground flaxseed to replace white or processed flours in muffins and other baked goods to increase fiber and protein.

4. Focus On Foods That Support Bone Health.

OEstrogen protects against bone loss, so when it starts to drop, women are at an increased risk for osteoporosis. This means that perimenopause is a very important time to support your bone health to prevent osteoporosis and its complications. You can do this in a few ways, but this first is by eating calcium-rich foods. If you choose and tolerate dairy, eat two servings per day and choose organic or grass-fed varieties. Plain or Greek yogurt are great options as they also contain live bacteria that support the gut. Skip sweetened and fruit-flavored yogurts and mix in chopped cucumber and fresh herbs instead of fruit as a savory snack. Plain cottage cheese and aged cheeses without additives or colorings are good sources of calcium and protein as well. If you don’t tolerate dairy, there are many nondairy calcium-rich foods to choose from. Try broccoli, bok choy, collard greens, kale, almonds, and canned salmon and sardines with bones. Many of these foods contain vitamin D, which helps your body absorb the calcium, but I find that most of my patients are who are defiecnet in Vit D need to supplement for optimal bone health—especially during perimenopause. To continue to support your bone health during perimenopause, ask your doctor to test your vitamin D levels and take a dose that’s right for you. Aim for 120 level. Two other often overlooked nutrients critical for bone health are magnesium and vitamin K2. Magnesium, found in nuts, legumes, leafy greens, and dark chocolate, is another mineral that makes up your bones. Vitamin K2, found in natto (fermented soy), egg yolks, cheese, and butter, tells your body to deposit the calcium in your bones, not your arteries or other organs. Just like vitamin D, food doesn’t typically provide an adequate amount of vitamin K2. Because of the emerging research on its role in bone health—as well as heart disease and diabetes—I recommend that women during and after perimenopause add a high-quality vitamin K2 supplement to their daily routine.

5. Don’t Forget Omega-3-Rich Foods.

During the transition to menopause, try to eat 4 ounces of omega-3-rich fish like salmon, sardines, tuna, mackerel, cod, and trout twice a week. Research shows that EPA and DHA, the two omega-3 fatty acids found in fish, reduce inflammation, improve mood, and reduce depression. They also reduce the risk for heart disease, another condition that women become at higher risk for after perimenopause. But what about plant-based omega-3s like walnuts and flaxseed? These foods contain the plant-based omega-3 ALA, which needs to be converted to EPA and DHA in order for you to receive the benefits. This means that nut-based omega-3s don’t replace fish-based ones, but they are still a great source of healthy fats and fiber. If you’re at an increased risk of heart disease or don’t like eating fish, ask your doctor about starting a high-quality fish oil supplement.

6. Eat More High-Fiber Complex Carbohydrates (Because Not All Carbs Are Bad).

Cutting out simple and processed sugars and replacing them with high-fiber complex carbohydrates will help balance your blood sugar during perimenopause. Healthy carbohydrates can also reduce mood swings, irritability, and depression and HOT Flushes. They increase the production of serotonin, one of the happy, feed-good hormones. I find that the best types and amounts of carbohydrates will vary from one person to another, as several things must be factored in like your medical history, activity level, and digestive health. If tolerated, beans, lentils, oats, quinoa, buckwheat, and other whole grains a few times a week are good options. Starchy vegetables like sweet potatoes, pumpkin , carrots, beets, winter squashes, and other root vegetables are great choices because they are rich in nutrients and fiber. By focusing on these foods—which can help decrease inflammation, support a healthy mood, and balance hormones and insulin levels—perimenopause doesn’t have to be something we dread. In fact, entering perimenopause is a great excuse to prioritize cooking at home, learning to love healthy foods and exercise, and generally taking a little extra care of yourself. That doesn’t sound like anything we should be afraid of!

Age-Related Cognitive Decline

Lets talk about an issue that all of us have to face after a certain point in our lives: COGNITIVE DECLINE.

 As we grow and develop from children to young adults, there is a palpable upward trend in our mental development and ability, and there is a sense that we are always growing to some greater height. Unfortunately, this trend can’t go on forever, and it is all too clear as the decades progress, that our minds are never going to be quite what they were. 


  • What is the process behind this gradual cognitive decline? 
  • What are the factors involved? Are there any in our control? 
  • Can we slow or stop this process in order to preserve our quality of life? 

Let’s break it down.


Cognitive decline is something that is generally known to happen as people age, but there are degrees of decline that can be considered excessive and unhealthy. 
There is no universally accepted definition of successful cognitive health in elderly individuals, but cognitive health is generally defined as “the development and preservation of the multidimensional cognitive structure that enables ongoing social connectedness, sense of purpose, and the ability to function independently” (1). That, broadly speaking, is the definition of the standard of cognitive ability that we all should be able to enjoy for our entire lives. 
Cognition encompasses a broad range of mental processes, which are often taken for granted until they are lost. There are two essential forms of cognition: 

  1. There is “fluid” cognition, which relies on short-term memory to process information when solving new problems, using spatial reasoning and when identifying patterns.
  2. There is also “crystallized” cognition, where knowledge and life experience accumulate, and this relies more on long-term memory (2)

Fluid cognitive abilities are thought to peak in the mid-twenties, and then very gradually decline over a period of years until about age 60, when the decline tends to become more rapid. But this is only for fluid cognition, while crystallized cognition continues to increase over the life span through education and life experiences.

Pathological cognitive decline is something that tends to be seen earlier than expected, or it hits the individual harder than expected, resulting in disruption of social connectedness, and individual autonomy. 

Mild Cognitive Impairment (MCI) is a condition presenting with memory deficits that are below what is considered normal. This condition can often foreshadow the onset of frank dementia, and early detection is very important, so that preventative measures may be taken to stem the progression of the condition.

Signs & Symptoms of MCI (Mild Cognitive Impairment)

Symptoms are often vague and can include the following:

  • Memory loss
  • Language disturbance (eg, difficulty in finding words)
  • Attention deficit (eg, difficulty in following or focusing on conversations)
  • Deterioration in visual-spatial skills (eg, disorientation in familiar surroundings in the absence of motor and sensory conditions that would account for the complaint) 

Cerebrovascular Conditions
Cerebrovascular disease (CVD) is defined as brain lesions caused by vascular disorders. This can be something as dramatic and severe as a stroke, where there is cessation of blood flow to a particular part of the brain, usually caused by a blood clot. But then there is also vascular dementia. 
Vascular dementia is a chronic progressive loss of cognitive function, due to multiple small infarcts (4). These can be thought of as very small mini-strokes that only affect minor sections of brain tissue at a time. By themselves, each one of these little infarcts doesn’t have a huge impact on cognitive function, as the brain is able to re-route to other neural pathways that bypass the section affected by the mini-stroke. 
However, over a period of years, as these mini-strokes accumulate, the available pathways the brain is left with become ever more restrictive, and so because of this you see a progressive decline in cognitive function.  

Prevalence of Dementia
In 2005, the global population suffering dementia was estimated to be 24.3 million people, and there are around 4.6 million new cases diagnosed every year (3). It is expected that this population will double every 20 years, with an alarming 81.1 million dementia patients in 2040 (3). A major consequence of this is an increased burden on the healthcare system, with higher rates of hospitalizations, surgeries and visits to the doctor, leading to spiraling healthcare costs.


Chronic systemic inflammation is the underlying culprit of many such chronic conditions, including heart disease, diabetes, cancer, and this very form of progressive damage to the brain. 

Increased chronic inflammation means greater chances of clotting factors activating, and causing the aforementioned “mini-strokes” that promote cognitive decline. Therefore, eating an anti-inflammatory Mediterranean type diet, avoiding simple sugar and carbs, avoiding fried foods and ensuring adequate intake of Omega 3 fatty acids, are some of the basic means of helping to preserve cognitive function as we mature.

In other words, less chronic inflammation, less clotting factors floating around in the system, less potential for oxidative damage, all equals less chance of a mini-clot causing these kinds of tiny infarcts in the brain.

There is a growing body of research demonstrating that adherence to a Mediterranean type diet significantly reduces risk of developing Mild Cognitive Decline, and risk of progression to Alzheimer’s Disease. (5)

In general, the Mediterranean diet, which is low calories and rich in fruits and vegetables, has the greatest benefit for reducing inflammation. Data show that high dietary fiber, which is typically a sign of a low glycemic load diet, was associated with lower levels of various inflammatory markers (6).
The dietary pattern most consistently associated with a reduction of CVD is predominantly plant-based, emphasizing fruits, vegetables, whole grains, nuts, fiber, and sources of Omega 3 fatty acids.


Cognitive Exercise
Another way to keep the brain functioning well, is just to make sure you are using it well. The brain tissue is very plastic, meaning that it always hast the ability to form new connections, and keep existing connections strong, as long as you challenge it with tasks to do. 
Evidence is not conclusive, but it is generally believed that exercising the brain by reading, doing crossword puzzles, and brain teasers can help to prevent, delay, or reduce cognitive decline. These should always be fun, stimulating activities that you enjoy doing, so that you will want to do them a lot.

Moderate Physical Exercise
Not only is moderate exercise a well established, and yet all too often overlooked, means of reducing chronic inflammation in the body (7), there is a growing body of evidence indicating that it can help prevent mild cognitive impairment as we age. 

Vitamin D
has been shown to be deficient or insufficient on pandemic levels, and lower levels are associated with several chronic diseases. It serves as a significant factor in a number of physiologic functions, specifically as a biological inhibitor of inflammatory hyperactivity (8, 9, 10). Vitamin D produces dose dependant reductions of several inflammatory markers, and supplemental benefit has been shown for osteoarthritis, multiple sclerosis, type 1 diabetes, Graves Disease, ankylosing spondylitis, SLE, and rheumatoid arthritis (8, 9, 10).
Data from the National Health and Nutrition Examination Survey (NHANES) from 2001-2004, involving more than 8000 human subjects, showed that those with vitamin D levels below 30 ng/ml were more likely to be at high risk of cardiovascular disease.

Fish Oil
A good quality fish oil supplement will be standardized to have large quantities of EPA and DHA, in a 3:1 or 3:2 ratio for adults. These omega 3 fatty acids promote the formation of anti-inflammatory eicosenoids that become incorporated into our cell membranes, helping them to remain fluid and pliable (11). This can help prevent heart disease and any associated cerebrovascular disease in the brain. 

Natural Antioxidants and Anti-inflammatories
Although a diet rich in fruits and vegetables is generally anti-inflammatory, some foods seem to exert some specific benefit along these lines. These include Blueberries (Vaccinium myrtillus), chocolate (dark), cranberries (Vaccinium macrocarpon), garlic (Alliu sativum), ginger (Zingiber officinalis), grape (Vitis vinifera), green tea (Camellia sinsensis), and turmeric (Curcuma longa).


NOVA Health Recovery | Alexandria, Va 22306 | Call for esketamine and nasal ketamine as well as IV Ketamine for depression, PTSD, anxiety  703-844-0184 < Link

Ketamine Virginia Link

Do Adjunctive Neutraceuticals Help Relieve Depression?

Using adjunctive neutraceuticals together with antidepressants can be helpful in reducing depressive symptoms, according to a new systematic review and meta-analysis published in the June 1, 2016 issue of the American Journal of Psychiatry.

An Australian research team analyzed findings of 40 studies encompassing 14 different neutraceuticals and found evidence to support the use of adjunctive S-adenosylmethionine (SAMe), methylfolate, omega-3 (primarily EPA or ethyl-EPA), and vitamin D in order to alleviate symptoms of depression.

Findings regarding omega-3 were particularly robust. Eight double blind RCTs of omega-3, varying in size (from 20 to 122 participants) and in duration (4 to 12 weeks), met inclusion criteria. Of these, 6 studies showed a statistically significant reduction in depression scores for the treatment group, compared to the placebo group, with a significant effect size of 0.61 (P=0.0009). Ten out of 15 datasets found an effect in favor of 1-carbon cycle neutraceuticals (which consist of SAMe, folic acid, methylfolate, B6, and B12).

Creatine and an amino acid combination yielded positive findings in “isolated studies,” and the researchers stated that these products should receive “tentative consideration.”

The investigators noted that further research is needed to clarify whether zinc, vitamin C, or tryptophan (more specifically, 5-HTP, the active precursor of serotonin) could be of value. They concluded that inositol is “unlikely to have any utility as an adjunctive antidepressant agent,” although some research has suggested it may have utility as depression monotherapy.

Studies were tabulated in 4 separate groups: 1-carbon cycle neutraceuticals (consisting of SAMe and folic acid or related forms, such as methylfolate, B6 and B12); omega-3; tryptophan; other neutraceuticals.

All of the investigated supplements have “mechanistic antidepressant activity underpinning their use,” the researchers emphasized. For example, 1-carbon cycle agents are critical in the methylation processes of monoamines. Omega-3 modulates norepinephrine, dopamine, and serotonin reuptake, degradation, synthesis, and receptor binding.

The study was undertaken in response to the “growing recognition that for many people with a depressive disorder, full remission is either short-lived or absent.” The researchers noted that augmentation and combination approaches with pharmaceuticals are often used in clinical practice. Coadministration of neutraceuticals may “provide an effective and safe approach to enhancing antidepressant effects” either by “synergistically augmenting an antidepressant agent” or by providing “a range of additional biological effects.”

Sarris J, Murphy J, Mischoulon D, et al. Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses. Am J Psychiatry. 2016;173(6):575-87.

Natural Depression Remedies

Natural protocol for depression treatment that includes omega-3s, magnesium, B vitamins, vitamin D, St John’s wort, ginkgo, SAMe, 5-HTP, and ginseng

Depression is a common mental disorder that presents with some or all of the following symptoms: a depressed mood, a loss of interest in things that once brought pleasure, feelings of guilt or low self-worth, disturbed sleep patterns, changes in appetite, a lack of energy, and poor concentration. These symptoms lead to impairments in an individual’s ability to take care of his or her everyday responsibilities and can become chronic or recurrent.   According the World Health Organization (WHO), depression is common worldwide, affecting about 121 million people. Untreated depression can lead to suicide, and the WHO estimates that 850,000 people worldwide commit suicide every year. Depression is the leading cause of disability worldwide and was the 4th leading contributor to the global burden of disease for the year 2000, according to the WHO. Their estimates project that depression will rise to 2nd place in the global burden of disease listing by the year 2020.  In many patients, mild to moderate depression can be successfully treated with a variety of naturopathic and holistic options, such as dietary changes, dietary supplements, exercise, massage, herbs, and sunlight.  Naturopathic medicine is based on the philosophy of addressing the basic underlying cause of any health condition. Proper nutrition is a foundational component of any natural medicine program. Nutrition affects mood through the many substrates and nutrients needed for proper neurotransmitter synthesis and function. A healthy diet is not only essential for proper neurotransmitter balance, but it affects the immune system in ways that then affect neurotransmitter function. The inclusion of exercise is also of utmost importance in any program addressing mood disorders. In addition to nutritional intervention and exercise, there are many other therapies that may improve mood in patients with mild depression. Following are a number of evidence-based, effective alternative/naturopathic treatments for depression, including dietary supplements, massage, herbs, sunlight, and more.

Anthroposophic Therapy

Anthroposophy is a spiritual science whose practical applications include biodynamic agriculture, anthroposophical medicinal products, and eurhythmy (“movement as visible speech”). Anthroposophic therapy is rooted in a healing method known as anthroposophical medicine, a branch of anthroposophic philosophy founded by Austrian philosopher and social thinker Rudolph Steiner in the 1920s. It utilizes a holistic approach, endeavoring to restore the balance between the physical, mental, and emotional states of the patient. Anthroposophical practitioners use medicines based on homeopathic principles and physical therapies that call upon massage and artistic expression to trigger the patient’s self-healing capacity. Anthroposophic medicine uses the anthroposophic view of the human being as a blend of 3 interdependent aspects: the physical body; the life force, understood as the source of growth and regeneration and sometimes called the soul; and the “astral body,” which mediates between the body and the soul, also called the “ego” or “consciousness.”  A 4-year study of the effectiveness of anthroposophic therapies in the treatment of depression evaluated 97 outpatients from 42 medical practices in Germany. Patients ranged from 20 to 69 years old and were referred to anthroposophic therapies (art, eurhythmy movement exercises, or rhythmical massage) or started physician-provided anthroposophic therapy (counseling, medication) for depression. Participants had suffered from depressed mood and at least 2 of 6 further depressive symptoms for a minimum of 6 months. Data were collected from July 1998 to March 2005.  The authors concluded “in outpatients with chronic depression, anthroposophic therapies were followed by long-term clinical improvement. Although the pre-post design of the present study does not allow for conclusions about comparative effectiveness, study findings suggest that the anthroposophic approach, with its recourse to nonverbal and artistic exercising therapies can be useful for patients motivated for such therapies.”1

Aromatherapy Massage

Aromatherapy is the use of essential oils to treat a variety of conditions. Naturopathic physicians use aromatherapy to treat depression, anxiety, insomnia, and stress-related disorders and to manage chronic pain.  Essential oils have been used effectively for centuries as a traditional medicine, but they have been the subject of few studies. Even in the absence of sufficient studies to completely explain the pharmacological effects of many essential oils or their active chemical constituents, the studies that have been done show measurable pharmacological effects when essential oils enter the blood stream through either inhalation or topical application.  Researchers at the Medicinal Plant Research Centre, United Kingdom, reviewed the published clinical trials of “psychoaromatherapy” in relation to psychiatric disorders, as well as evidence from mechanistic, neuropharmacological studies of the effects of essential oils. The authors concluded that aromatherapy may offer effective treatment for a range of psychiatric disorders. They also found that it does not appear to pose the risk of adverse effects found with many conventional psychotropic drugs.2 Various aromatherapy oils, diluted in carrier oil like almond or olive oil, are massaged into the skin, where they are absorbed into the bloodstream. Below is a list of some of the essential oils used in the treatment of depression and anxiety.

  • Clary sage is used for treating insomnia, anxiety, and depression.
  • Basil lifts fatigue, anxiety, and depression.
  • Rose acts on the nervous system.
  • Ylang ylang is used for anxiety, depression, insomnia, and stress.
  • Sandalwood has sedative properties and is good for treating depression and tension.
  • Lavender is used for depression, headache, hypertension, insomnia, migraine, nervous tension, and other stress-related conditions.
  • Jasmine increases the beta waves in the frontal lobe, which can create a more alert and responsive state of mind.
  • Rosemary relieves headaches and aids clear thinking.
  • Patchouli has an uplifting effect for depression and anxiety.
  • Chamomile is very calming; it soothes nerves and helps insomnia.
  • Geranium is both sedative and uplifting and thus is used for treating nervous tension, depression, and hormonal and menstrual problems.

 A 2007 clinical study published in the Journal of Clinical Oncology looked at the effectiveness of aromatherapy massage in the management of anxiety and depression in patients with cancer. Two hundred eighty-eight cancer patients in the United Kingdom referred to complementary therapy services because of clinical anxiety and/or depression were randomized to a course of aromatherapy massage or usual supportive care alone. The authors concluded that aromatherapy massage does not appear to confer benefit on cancer patients’ anxiety and/or depression in the long term but is associated with clinically important benefit up to 2 weeks after the intervention.3 In other words, aromatherapy is not a cure for depression, but it may be an effective short-term aid in managing depression and anxiety when used with other treatment options. According the World Health Organization (WHO), depression is common worldwide, affecting about 121 million people.Another study was conducted with nursing students in Korea to test the effectiveness of lavender essential oil on insomnia and depression. In a 4-week-long, single-blind, repeated-measurements experiment, researchers studied 42 female students who complained of insomnia. The lavender fragrance had a beneficial effect on insomnia and depression in the students, though repeated studies would be needed to confirm effective proportions of lavender oil and carrier oil for insomnia and depression.4 A controlled trial conducted in Thailand tested the relaxation properties of ylang ylang oil. The oil caused a significant decrease in blood pressure, a significant increase in skin temperature, and a greater sense of calm and more relaxation. The authors conclude that there is evidence of the effectiveness of ylang ylang oil for relief of depression and stress in humans.5

Dietary Changes/Supplements

The first line of naturopathic treatment for almost every disease is improved patient nutrition. Nutrition plays a key role in the onset, severity, and duration of depression, including daily mood swings. Food patterns preceding the onset of depression and during a depressive episode are similar. These patterns may include skipping meals, poor appetite, and a desire for sweets. Depressive symptoms are exacerbated by nutritional imbalances, including 

  • frequent consumption of caffeine;
  • sucrose consumption;
  • deficiencies in vitamins and minerals (biotin, folic acid, and other B vitamins; vitamin C; calcium; copper; iron; magnesium; or potassium);
  • excesses of vanadium6,7;
  • imbalances in amino acids; and
  • food allergies.

A recent study published in Neuropharmocology demonstrates that physiologically relevant doses of caffeine can significantly depress adult hippocampal neurogenesis.8 (Adult neurogenesis has been associated with learning, memory, and depression). A review published by the Oklahoma State Medical Association finds that “caffeine is a widely used psychoactive substance that has the potential to contribute to many psychiatric symptoms.”9 Sugar intake has been linked to depression. In an article in the Journal of Depression and Anxiety, the national rate of sugar consumption was shown to directly affect the prevalence of major depression. The basis for this includes the relationship between sugar consumption, β-endorphins, and oxidative stress.10

Dietary Recommendations

The main dietary focus in treating depression is to ensure that the patient’s diet is rich in foods containing omega-3 fatty acids and those containing magnesium, vitamins B and D, and the antioxidant vitamins A, C, and E. Along with proper food, sufficient water intake plays a vital role in maintaining proper chemical balance in the body; even mild dehydration can cause fatigue. The Institute of Medicine advises that women should consume 2.7 Ls (91 oz) of total water (from all beverages and foods) each day, and men should average approximately 3.7 L (125 oz daily) of total water. The panel did not set an upper limit for water consumption.11

Omega-3 Fatty Acids

Foods that are rich in omega-3 fatty acids have been shown to reduce neuronal phospholipid turnover. In 1 study, registered difference images showed that the “omega-3 treatment was accompanied by structural brain changes including, in particular, a reduction in the lateral ventricular volume.”12 A 2007 meta-analysis of trials involving patients with major depressive disorder and bipolar disorder provided evidence that omega-3 PUFA supplementation reduces symptoms of depression.13 The foods with the highest amounts of omega 3 are flax seeds, Chia seeds, walnuts, baked/broiled salmon, soybeans, baked/broiled halibut, sardines, herring, tofu, and winter squash. Other foods containing omega-3s are canola oil, olive oil, broccoli, cantaloupe, kidney beans, spinach, grape leaves, Chinese cabbage, and cauliflower.

Dietary Magnesium

Studies have shown an inverse relationship between magnesium intake and depression and anxiety.14-16 Patients with depression should add foods that are high in magnesium to their diet, such as fish, barley, artichokes, buckwheat, oat bran, almonds, cashews, pine nuts, black beans, white beans, cornmeal, spinach, broccoli, tomatoes, pumpkin seeds, and soybeans. Whole-wheat flour contains magnesium, but the magnesium-rich germ and bran are removed in the process of making white flour. All green vegetables are sources of magnesium because the center of the chlorophyll molecule contains magnesium.

B Vitamins

The B-complex vitamins are water-soluble vitamins that are essential to mental and emotional well-being. B-vitamin deficiency is common because B vitamins are easily destroyed by common lifestyle behaviors such as drinking alcohol and caffeinated beverages, smoking, and eating foods rich in refined sugars. Studies have shown that vitamin-B deficiency can be a cause of both depression and epilepsy and that “preventive vitamin B supplementation and sufficient intake seem very important for secondary and primary prevention of neuropsychiatric disorders, especially in subjects with a low intake or status of the vitamins.”17 When advising patients to supplement with specific B vitamins, it must be remembered that the patient must also take a B-complex supplement to prevent imbalances. Nerve tissue requires vitamin B1 to utilize glucose to produce energy; this vitamin modulates cognitive performance, especially in the elderly. Folic acid preserves the brain during its development and preserves memory during aging. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B6 is likely to benefit the treatment of premenstrual depression. Good sources of B vitamins include the following.

  • Asparagus, broccoli, spinach, bananas, potatoes
  • Dried apricots, dates, and figs
  • Milk, eggs, cheese, yogurt
  • Nuts and legumes (includes rice, corn, soy beans, string beans, peas, lentils, mustard, sesame seeds, and poppy seeds)
  • Fish
  • Brown rice, wheat germ, whole grain cereals

Vitamin D

Seasonal affective disorder (SAD) is prevalent when vitamin D stores are typically low. Researchers note that people suffering from depression, particularly those with SAD, tend to improve as their levels of vitamin D in the body increase.18 It has been hypothesized that vitamin D increases levels of serotonin in the brain.19 There are individual differences in the amount of vitamin D needed daily based on geographical location, the time of year, skin type, and amount of sun exposure. Research is ongoing to establish new standards for recommended daily vitamin D intake for adults as the importance of proper vitamin D levels becomes more obvious; currently, tolerable upper intake levels for vitamin D according to the National Institutes of Health Office of Dietary Supplements is 2,000 IU for adults and children over the age of 13 and 1,000 IU for children under one year of age.20 In an experiment conducted in 1998, Australian researchers found that vitamin D3(cholecalciferol) given in doses of 400 IU and 800 IU had significant positive effects on the mood of healthy individuals. Forty-four people were given either 400 IU of vitamin D, 800 IU of vitamin D, or a placebo for 5 days during the late winter. Research subjects reported that vitamin D3 had the effect of enhancing a positive mood and also reducing a negative mood in some cases. The authors concluded, “Vitamin D3 deficiency provides a compelling and parsimonious explanation for seasonal variations in mood.”21 In 1999, a study done by Hollis, Gloth, and Alam showed that a one-time dose of 100,000 IU of vitamin D improved symptoms of depression better than light therapy in a small group of participants who suffered from SAD.22 All of the participants in the vitamin D group improved according to all depression scale measurements, and the increase of serum 25-hydroxyvitamin D [25-(OH)D] levels was strongly associated with the degree of improvement of SAD symptoms. A study at the Institute of Clinical Medicine in Norway examined the relationship between serum 25-(OH)D levels and depression in overweight and obese subjects and assessed the effect of vitamin D supplementation on depressive symptoms. Researchers found a significant improvement in Beck Depression Inventory scores after 1 year in the 2 groups given vitamin D but not in the placebo group. There was a significant decrease in serum parathyroid hormone in the 2 vitamin D groups without a concomitant increase in serum calcium. There are receptors for parathyroid hormone (PTH) and 1,25–dihydroxyvitamin D in the brain, and there are clinical and experimental data indicating that PTH and vitamin D may affect cerebral function.22 The authors concluded that there “appears to be a relation between serum levels of 25-(OH) D and symptoms of depression. Supplementation with high doses of vitamin D seems to ameliorate these symptoms indicating a possible causal relationship.”23  Dietary sources of vitamin D include milk, salmon, and tuna. The best food source of vitamin D is salmon, with 530 IU per 3 oz of canned salmon. Salmon is also rich in omega 3 fatty acids, making it a very important part of a depression prevention or treatment diet.


Research has shown that exercise is an effective but often underused treatment for mild to moderate depression, even in elderly patients, and has virtually no side effects.24,25Researchers at Duke University demonstrated several years ago that exercise can be an effective antidepressant even for those patients with major depressive disorder.26 According to a report from the UK Mental Health Foundation, exercise may be just as effective at treating depression as antidepressant medicines, and they also claim that being physically active may help prevent depression in the first place. The UK report also states that exercise therapy should be used as a first-line treatment for mild depression because it may be just as effective as antidepressant medicines.27 Exercise has a number of beneficial physiological effects that make it ideal for treating depression. Exercise has been proven to increase activity in both the frontal lobe of the brain and the hippocampus. It also has been found to increase mood-enhancing brain-derived neurotrophic factor levels.28,29 Studies have also found that exercise increases levels of serotonin, dopamine, and norepinephrine.30-35 Physical activity should last at least 20 minutes a session for at least 10 weeks in order to help improve psychological well-being. Aerobic activities such as brisk walking, jogging, cycling, swimming, and dancing tend to be the most effective for treating depression.36

Natural Medicines

Several herbs have been proven to have a beneficial effect on depression and its symptoms of anxiety, sleeplessness, and inability to concentrate. Following are some of the most common herbs and supplements used for mild to moderate depression.

St John’s Wort (Hypericum perforatum

St John’s wort is a bushy plant with a turpentine-like odor and yellow flowers whose petals have black dots on the margins. Its extract has been used in various folk remedies and herbal tinctures since Roman times. It is used extensively in both the United States and Europe to treat mild to moderate depression. A German study compared the effectiveness of St John’s wort with imipramine, a well-known antidepressant. The trials involved 40 outpatient clinics in Germany with a total of 324 outpatients suffering mild to moderate depression. Participants were given either 75 mg imipramine twice daily or 250 mg Hyericum perforatum extract  ZE 117 twice daily for 6 weeks. The study concluded that H perforatum extract is therapeutically equivalent to imipramine in treating mild to moderate depression and is better tolerated.37 Another German review investigated the efficacy and side effects of H perforatum. This study looked at 27 trials that included a total of 2,291 patients who met inclusion criteria. Seventeen trials, with a total of 1,168 patients, were placebo-controlled (16 addressed single preparations, 1 a combination with 4 other plant extracts). Ten trials (8 single preparations, 2 combinations of Hypericum and Valeriana) with a total of 1,123 patients compared Hypericum with other antidepressant or sedative drugs. Most trials were 4 to 6 weeks long. Participants usually had “neurotic depression” or “mild to moderate severe depressive disorders.” The study concluded that “there is evidence that extracts of Hypericum are more effective than placebo for the short-term treatment of mild to moderately severe depressive disorders.” The proportions of patients reporting side effects were 26.3% for Hypericum single preparations vs 44.7% for standard antidepressants and 14.6% for combinations vs 26.5% with amitriptyline or desipramine. In other words, patients taking standard antidepressant medications were almost twice as likely to experience side effects as patients taking Hypericum.38 Until 2004, only 1 randomized controlled trial had been conducted using Hypericum in patients with severe depression, but it was underpowered and so its negative findings were questionable.39 With this in mind, German researchers conducted a study of acute treatment of moderate to severe depression with Hypericum extract WS 5570 vs paroxetine. The study involved 251 adult outpatients with acute major depression with total score ≥22 on the 17-item Hamilton Depression Scale from 21 psychiatric primary care practices in Germany. Patients were given either 900 mg/day Hypericum extract WS 5570 (300 mg 3 times/d) or 20 mg paroxetine once per day for 6 weeks. (In initial nonresponders, doses were increased to 1,800 mg/day Hypericum or 40 mg/day paroxetine after 2 weeks.) The study concluded that Hypericum extract WS 5570 is at least as effective as paroxetine in the treatment of moderate to severe major depression and is better tolerated.40 A comprehensive clinical review by British researchers supports the findings of the various studies above, and the authors note that all studies have found Hypericum to be less likely to cause side effects than standard pharmaceutical drugs used currently.41 The mechanism of action with St John’s wort is being investigated. Initial biochemical studies report that St John’s wort inhibits the uptake of serotonin, dopamine, and noradrenalin (norepinephrine). However, other in vitro binding assays carried out using St John’s wort extract demonstrate significant affinity for adenosine, GABA (A), GABA (B), and glutamate receptors. In vivo, St John’s wort extract leads to a decrease in the number of beta-adrenergic receptors and an increase in the number of serotonin 5-HT(2) receptors in the rat frontal cortex and causes changes in neurotransmitter concentrations in brain areas that are implicated in depression. However, there are reasons to be cautious when prescribing St John’s wort, as it has been found to have significant interactions with some other drugs. In a study done at the College of Pharmacy in Little Rock, Arkansas, comparisons of pre– and post–St John’s wort phenotypic ratios revealed significant induction of CYP3A4 and CYP2E1 activity.42 Because CYP3A4 is involved in the oxidative metabolism of more than 50% of all drugs, this suggests that Hypericum extracts are likely to interact with many more drugs than previously had been realized. Examples of medications that could be affected include carbamazepine (anticonvulsant and analgesic), cyclosporine (immunosuppressant), irinotecan (cancer drug), midazolam (anesthetic), nifedipine (calcium channel blocker), birth control pills, simvastatin (cholesterol-lowering drug), theophylline (bronchodilator), tricyclic antidepressants, warfarin (blood thinner), or HIV drugs such as nonnucleoside reverse transcriptase inhibitors or protease inhibitors. St John’s wort may also interact with digoxin or digitoxin (cardiac drug), resulting in a decrease in digoxin blood concentration. There may also be an interaction with triptan-type headache medications. Examples include naratriptan, rizatriptan, sumatriptan, and zolmitriptan. In theory, St John’s wort may also interact with certain chemotherapy drugs such as anthracyclines and may increase antiinflammatory effects of COX-2 inhibitor drugs or nonsteroidal antiiflammatories such as ibuprofen. 

Ginkgo Biloba

The Ginkgo biloba tree is an ancient species of tree native to the Asia. Chinese herbalists have used ginkgo for thousands of years, and it is one of the most widely studied botanical products. Ginkgo is widely used throughout both the United States and Europe. Since ginkgo nuts are mildly toxic, most of the ginkgo sold is in the form of a standardized extract of the leaves of the tree.  Ginkgo has a long history in traditional medicine for treating circulatory disorders and enhancing memory. Scientific studies throughout the years support the effectiveness of ginkgo for these problems.43-48 Evidence to date shows that ginkgo biloba extract (GBE) is primarily effective in the elderly and when treating disorders that are caused by diminished cerebral blood flow. Laboratory studies have shown that “GBE improves blood circulation by dilating blood vessels and reducing the stickiness of blood platelets.” Ginkgo leaves also contain flavonoids and terpenoids, which are powerful antioxidants.49,50Ginkgo biloba can be used to enhance other depression treatments and sometimes can be used alone instead of pharmaceutical treatments for mild cases of depression. Even in cases where ginkgo is used as an adjunct to other depression treatments, it can be helpful as an aid to improving short-term memory by improving cerebral circulation.


S-adenosylmethionine is sold as a nutritional supplement under the marketing name SAMe. SAMe is also marketed as an approved prescription drug in Russia, Italy, and Germany. The supplement SAMe is a synthetic form of a compound formed naturally in the body from the essential amino acid methionine and adenosine triphosphate. It was first discovered in 1953. SAMe serves as a primary methyl group donor in various physiological reactions and is then converted to S-adenosyl-homocysteine.51-54 Clinical trials have shown that SAMe is effective in treating depression when taken on a regular basis. Other conditions that SAMe has been shown to help in clinical trials are liver disease and osteoarthritis. SAMe is required for the biosynthesis of the neurotransmitters dopamine and serotonin as well as for cellular growth and repair. Patients with bipolar disorder or anxiety disorders or other psychiatric disease must be closely monitored while taking SAMe as it has been associated with hypomania and mania. There are also concerns that SAMe could cause levodopa to be less effective when taken over a long period of time, so patients with Parkinson’s disease should be advised to avoid this supplement.55 There are a number of side effects associated with SAMe; the most commonly reported are nausea and other digestive disturbances. Less common side effects include anxiety, insomnia, increased thirst, increased urination, headache, hyperactivity, decreased blood glucose levels, skin rashes, dry mouth, and blood in the stool. Therapeutic doses range from 400 mg per day to 1,600 mg per day, although higher doses are used empirically in some cases. In contrast, some physicians recommend lower doses ranging from 50 to 200 mg per day to treat mild depression in an effort to lessen the risk of triggering the side effects mentioned above.


5-Hydroxytryptophan (5-HTP) is a naturally occurring amino acid, a precursor to the neurotransmitter serotonin, and an intermediate in tryptophan metabolism. 5-HTP is effective in treating depression, suppressing appetite, and promoting sleep. 5-HTP increases serotonin synthesis and release, making it useful in the treatment of conditions thought to be caused or made worse by a lack of serotonin. Care must be used to avoid serotonin syndrome in patients taking antidepressant medications. 5-HTP is usually extracted from the seeds of Griffonia simplicifolia and sold in 50 mg or 100 mg gelatin or vegetarian capsules. 

Siberian ginseng (Eleutherococcus senticosus)

Siberian ginseng, also known as Eleuthero, is an adaptogen that has been used for centuries in eastern countries, including China and Russia. As an adaptogen, it helps to control excess cortisol levels and thereby reduces depression.56,57 Although a distant relative of American ginseng (Panax quinquefolius) and Asian ginseng (Panax ginseng) with some overlap in its uses, Siberian ginseng is a distinct plant with different active chemical components. Ten compounds have been isolated from Siberian ginseng. Its pharmacological activities are mainly due to lignans and iridoid glycosides, such as eleutherosides.58Prized for its ability to restore vigor, increase longevity, enhance overall health, and stimulate both a healthy appetite and a good memory, it is widely used in Russia to help the body adapt to stressful conditions and to enhance productivity.  Practitioners of Chinese medicine use Siberian ginseng to restore the balance of qi and to treat a deficiency of yang in the spleen and kidney. Siberian ginseng is also an antioxidant, a nervine, an anticholesteremic, and mildly antiinflammatory. Siberian ginseng is used to help the body deal with physical and mental stressors such as heat, cold, physical exhaustion, viruses, bacteria, chemicals, extreme working conditions, noise, and pollution. It works by strengthening the system, thereby helping to prevent illness. It has been shown to have significant antidepressant effects in rats that were subjected to the desperation test and neuropharmacological tests based on the antagonist activity with respect to reserpine clofelin, and L-DOPA,59 and a Chinese study has shown that Siberian ginseng exhibited antifatigue, antistress, immunoenhancing effect, central nervous system activity, and antidepressive effects.60


Phototherapy is the use of light to treat disease and is a treatment of choice for SAD. Other indications for bright light therapy include nonseasonal depression, bipolar depression, chronic depressive disorder, antepartum and postpartum depression, late luteal phase dysphoric disorder, circadian phase sleep disorders, jet lag, shift work problems, and behavioral disturbance and insomnia in organic dementia. A 2004 study combining bright light exposure and physical exercise showed that this treatment may be an effective way of relieving depressive symptoms. The study concluded that “problems with sleep, especially initial insomnia, may predict a good response to treatment using combined light and exercise. Bright light exposure and physical exercise, even in combination, seem to be well tolerated and effective on depressive symptoms.”61 At the Be’er Ya’akov Mental Health Center associated with Tel Aviv University, Israel, a pilot study was conducted using partial sleep deprivation during the second half of the night, medium (green) wavelength light in combination with dawn simulation, bright light therapy, and sleep phase advance. The results showed the procedure to be effective and well tolerated. It affords many advantages, such as “the achievement of a rapid response, no extinction of the therapeutic effect after 4 weeks of follow-up, safety, high patient compliance, and cost effectiveness.”62

Energy Psychology

Many of the body’s electrical systems and energy fields are understood, readily verified, and a focus of established interventions. The application of lasers and magnetic pulsation, for example, can be described in terms of specific, measurable wavelengths and frequencies that have been found to be therapeutic.63 Other energies are considered to be of a more subtle nature and have not been directly measured by reproducible methods. While such subtle energies are generally not recognized in Western healthcare frameworks, they are at the root of numerous ancient systems of healing and spiritual development that are not only still in wide use throughout the world but increasingly being utilized in the West. Energy psychology has been referred to as “acupuncture without needles” in treating mental health disorders. More than two dozen variations of energy psychology can be identified, with the most well-known being Thought Field Therapy (TFT), the Tapas Acupressure Technique (TAT), and the Emotional Freedom Techniques (EFT). Many of these adapt practices and concepts from acupuncture and acupressure; others borrow from yoga, meditation, qigong, and other traditional practices. Some practitioners of these modalities describe their therapeutic mechanism as the activation of electrical signals that are said to influence brain activity64; others as describe them as catalyzing shifts in putative energy fields, such as the body’s biofield.65TFT, TAT, and EFT, each utilizing techniques derived from acupuncture and acupressure, have received by far the most attention. But what is the proof that there is any real effectiveness to these methods? Evidence is still preliminary, but energy psychology is gaining credence as an evidence-based treatment. In fact, 1 form has met the American Psychological Association’s criteria as a “probably efficacious treatment” for specific phobias; another has met the criteria for maintaining weight loss.66 The limited scientific evidence, combined with extensive clinical reports, suggests that energy psychology holds promise as a rapid and potent treatment for a range of psychological conditions. 


A number of alternatives to standard antidepressant medications exist for patients with mild to moderate depression. An essential first step is to work with the patient to ensure proper diet and regular exercise. Once this has been done, nutritional supplementation, herbal medicines, phototherapy, and energy psychologies can be utilized according to patient needs as described above. 

About the Author

Rena Freedenberg, ND, graduated from Michlelet Eden College of Natural Medicine in Jerusalem, Israel, where she did 2 years of internship in internal medicine. Freedenberg’s practice is located in Beitar Illit, Israel, where she specializes in women’s and children’s healthcare. Her primary interest is in addressing the underlying causes of illness and improving the health and quality of life of women and their families.


  1. Hamre HJ, Witt CM, Glockmann A, et al. Anthroposophic therapy for chronic depression: a four-year prospective cohort study. BMC Psychiatry. 2006; 6:57. 
  2. Perry N, Perry E. Aromatherapy in the management of psychiatric disorders: clinical and neuropharmacological perspectives. CNS Drugs. 2006;20(4):257-280.
  3. Wilkinson SM, Love SB, Westcombe AM, et al. Effectiveness of aromatherapy massage in the management of anxiety and depression in patients with cancer: a multicenter randomized controlled trial. J Clin Oncol. 2007;25(5):532-539.
  4. Lee IS, Lee GJ. Effects of lavender aromatherapy on insomnia and depression in women college students. Taehan Kanho Hakhoe Chi. 2006;36(1):136-143.
  5. Hongratanaworakit T, Buchbauer G. Relaxing effect of ylang ylang oil on humans after transdermal absorption. Phytother Res. 2006;20(9):758-763.
  6. Naylor GJ, Smith AH. Vanadium: a possible aetiological factor in manic depressive illness. Psychol Med. 1981;11(2):249-256.
  7. Naylor GJ. Vanadium and manic depressive psychosis. Nutr Health. 1984;3(1-2):79-85.
  8. Wentz CT, Magavi SS. Caffeine alters proliferation of neuronal precursors in the adult hippocampus. Neuropharmacology. 2009; 56(6-7):994-1000. 
  9. Broderick P, Benjamin AB. Caffeine and psychiatric symptoms: a review. J Okla State Med Assoc. 2004;97(12):538-542
  10. Westover AN, Marangell LB. A cross-national relationship between sugar consumption and depression? J Depression Anxiety. 2002;16:118-120.
  11. Panel on Dietary Reference Intakes for Electrolytes and Water, Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes: Water, Potassium, Sodium, Chloride, and Sulfate. Released February 11, 2004.
  12. Puri BK, Counsell SJ, Hamilton G, Richardson AJ, Horrobin DF. Eicosapentaenoic acid in treatment-resistant depression associated with symptom remission, structural brain changes and reduced neuronal phospholipid turnover. Int J Clin Pract. 2001;55(8):560-563.
  13. Ross BM, Seguin J, Sieswerda LE. Omega-3 fatty acids as treatments for mental illness: which disorder and which fatty acid? Lipids Health Dis. 2007:6:21. 
  14. Jacka FN, Overland S, Stewart R, et al. Association between magnesium intake and depression and anxiety in community-dwelling adults: the Hordaland Health Study. Aust N Z J Psychiatry. 2009;43(1):45-52.
  15. Jung KI, Ock SM, Chung JH, Song CH. Associations of serum Ca and Mg levels with mental health in adult women without psychiatric disorders. Biol Trace Elem Res. 2009 Jun 19 [epub ahead of print].
  16. Eby GA, Eby KL. Rapid recovery from major depression using magnesium treatment. Med Hypotheses. 2006;67(2):362-370.
  17. Herrmann W, Lorenzl S, Obeid R. Review of the role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric disorders—current evidence and preliminary recommendations. Fortschr Neurol Psychiatr. 2007;75(9):515-527.
  18. Gloth FM 3rd, Alam W, Hollis B. Vitamin D vs broad spectrum phototherapy in the treatment of seasonal affective disorder. J Nutr Health Aging. 1999;3(1):5-7.
  19. Partonen T. Vitamin D and serotonin in winter. Med Hypotheses. 1998;51(3):267-268.
  20. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academy Press, 1997.
  21. Lansdowne AT, Provost SC. Vitamin D3 enhances mood in healthy subjects during winter. Psychopharmacology (Berl). 1998;135(4):319-323.
  22. Jorde R, Waterloo K, Saleh F, Haug E, Svartberg J. Neuropsychological function in relation to serum parathyroid hormone and serum 25-hydroxyvitamin D levels. The Tromsø study. J Neurol. 2006;253(4):464-470. 
  23. Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. J Intern Med. 2008;264(6):599-609. 
  24. Rethorst CD, Wipfli BM, Landers DM. The antidepressive effects of exercise: a meta-analysis of randomized trials. Sports Med. 2009;39(6):491-511.
  25. Blumenthal JA, et al. Effects of exercise training on older patients with major depression. Arch Intern Med. 1999;159:2349-2356.
  26. Babyak M, Blumenthal JA, Herman S, et al. Exercise treatment for major depression: maintenance of therapeutic benefit at 10 months. Psychosom Med. 2000;62(5):633-638.
  27. Mental Health Foundation. Up and running: exercise therapy and the treatment of mild or moderate depression in primary care. 2005. November 20, 2009.
  28. Ni H, Li C, Tao LY, Cen JN. Physical exercise improves learning by modulating hippocampal mossy fiber sprouting and related gene expression in a developmental rat model of penicillin-induced recurrent epilepticus. Toxicol Lett. 2009 1;191(1):26-32. 
  29. Helfer JL, Goodlett CR, Greenough WT, Klintsova AY. The effects of exercise on adolescent hippocampal neurogenesis in a rat model of binge alcohol exposure during the brain growth spurt. Brain Res. 2009;1294:1-11.
  30. Caperuto EC, dos Santos RV, Mello MT, Costa Rosa LF. Effect of endurance training on hypothalamic serotonin concentration and performance. Clin Exp Pharmacol Physiol. 2009;36(2):189-191.
  31. Pothakos K, Kurz MJ, Lau YS. Restorative effect of endurance exercise on behavioral deficits in the chronic mouse model of Parkinson’s disease with severe neurodegeneration. BMC Neurosci. 2009;10:6.
  32. Farrell PA, Gustafson AB, Morgan WP, Pert CB. Enkephalins, catecholamines, and psychological mood alterations: effects of prolonged exercise. Med Sci Sports Exerc. 1987;19(4):347-53. 
  33. Kotchen TA, Hartley LH, Rice TW, Mougey EH, Jones LG, Mason JW. Renin, norepinephrine, and epinephrine responses to graded exercise. J Appl Physiol. 1971;31(2):178-184.
  34. Rasmussen P, Brassard P, Adser H. Evidence for a release of brain-derived neurotrophic factor from the brain during exercise. Exp Physiol. 2009;94(10):1062-1069. 
  35. BDNF brain-derived neurotrophic factor.[gene])%20AND%20(Homo%20sapiens[orgn])%20AND%20al
  36. Petruzzello SJ, Landers DM, et al. A meta-analysis on the anxiety-reducing effects of acute and chronic exercise. Outcomes and mechanisms. Sports Med.1991;11(3):143-182.
  37. Woelk H. Comparison of St. John’s wort and imipramine for treating depression: randomised controlled trial. BMJ. 2000;321(7260):536-539.
  38. Linde K, Mulrow CD. St. John’s wort for depression. Cochrane Database Syst Rev. 2000;(2):CD000448.
  39. Hypericum Depression Trial Study Group. Effect of Hypericum perforatum (St John’s wort) in major depressive disorder: a randomized controlled trial. JAMA. 2002;287(14):1807-1814. 
  40. Szegedi A, Kohnen R, Dienel A, Kieser M. Acute treatment of moderate to severe depression with hypericum extract WS 5570 (St John’s wort): randomised controlled double blind non-inferiority trial versus paroxetine. BMJ. 2005;330(7490):503.
  41. Whiskey E, Werneke U, Taylor D. A systematic review and meta-analysis of Hypericum perforatum in depression: a comprehensive clinical review. Int Clin Psychopharmacol. 2001;16(5):239-252.
  42. Gurley BJ, Gardner SF, Hubbard MA, et al. Clinical assessment of effects of botanical supplementation on cytochrome P450 phenotypes in the elderly: St. John’s wort, garlic oil, Panax ginseng and Ginkgo bilobaDrugs Aging. 2005;22(6):525-539.
  43. Wu YZ, Li SQ, Zu XG, Du J, Wang FF. Ginkgo biloba extract improves coronary artery circulation in patients with coronary artery disease: contribution of plasma nitric oxide and endothelin-1. Phytother Res. 2008;22(6):734-739.
  44. Boelsma E, Lamers RJ, Hendriks HF, van Nesselrooij JH, Roza L. Evidence of the regulatory effect of Ginkgo biloba extract on skin blood flow and study of its effects on urinary metabolites in healthy humans. Planta Med. 2004;70(11):1052-1057.
  45. Kasper S, Schubert H. Ginkgo biloba extract EGb 761 in the treatment of dementia: evidence of efficacy and tolerability. Fortschr Neurol Psychiatr. 2009;77(9):494-506.
  46. Cho HJ, Shon YH, Nam KS. Ginkgolide C inhibits platelet aggregation in cAMP- and cGMP-dependent manner by activating MMP-9. Biol Pharm Bull. 2007;30(12):2340-2344.
  47. Pietta PG. Flavonoids as antioxidants. J Nat Prod. 2000;63(7):1035-1042.
  48. Grassmann J. Terpenoids as plant antioxidants. Vitam Horm. 2005;72:505-535.
  49. Blecharz-Klin K, Piechal A, Joniec I, Pyrzanowska J, Widy-Tyszkiewicz E. Pharmacological and biochemical effects of Ginkgo biloba extract on learning, memory consolidation and motor activity in old rats. Neurobiol Exp (Wars). 2009;69(2):217-231.
  50. Cho HJ, Shon YH, Nam KS. Ginkgolide C inhibits platelet aggregation in cAMP- and cGMP-dependent manner by activating MMP-9. Biol Pharm Bull. 2007;30(12):2340-2344. 
  51. Knowlton L. Investigating SAM-e. Geriatric Times. 2001:2(5). 2001. Accessed November 20, 2009.
  52. Kagan BL, Sultzer DL, Rosenlicht N, Gerner RH. Oral S-adenosylmethionine in depression: a randomized, double-blind, placebo-controlled trial. Am J Psychiatry. 1990;147(5):591-595.
  53. Rosenbaum JF, Fava M, Falk WE, et al. The antidepressant potential of oral S-adenosyl-l-methionine. Acta Psychiatr Scand. 1990;81(5):432-436. 
  54. Hardy ML, Coulter I, Morton SC, et al. S-adenosyl-L-methionine for treatment of depression, osteoarthritis, and liver disease. Evid Rep Technol Assess (Summ). 2003;(64):1-3.
  55. Liu X, Lamango N, Charlton C. L-dopa depletes S-adenosylmethionine and increases S-adenosyl homocysteine: Relationship to the wearing off effects. Soc Neurosci. 1998;24:1469.
  56. Panossian A, Wikman G. Evidence-based efficacy of adaptogens in fatigue, and molecular mechanisms related to their stress-protective activity. Curr Clin Pharmacol. 2009;4(3):198-219.
  57. Römer B, Lewicka S, Kopf D, et al. Cortisol metabolism in depressed patients and healthy controls. Neuroendocrinology. 2009;90(3):301-306.
  58. Deyama T, Nishibe S, Nakazawa Y. Constituents and pharmacological effects of Eucommia and Siberian ginseng. Acta Pharmacol Sin. 2001;22(12):1057-1070.
  59. Kurkin VA, Dubishchev AV, Ezhkov VN, et al. Antidepressant activity of some phytopharmaceuticals and phenylpropanoids. Pharmaceut Chem J. 2006. 40(11):33-38.
  60. Deyama T, Nishibe S, Nakazawa Y. Constituents and pharmacological effects of Eucommia and Siberian ginseng. Acta Pharmacol Sin. 2001;22(12):1057-1070.
  61. Leppämäki S, Haukka J, Lönnqvist J, Partonen T. Drop-out and mood improvement: a randomised controlled trial with light exposure and physical exercise. BMC Psychiatry. 2004;4:22. 
  62. Moscovici L, Kotler M. A multistage chronobiologic intervention for the treatment of depression: a pilot study. J Affect Disord. 2009;116(3):201-207.
  63. Oschman J. Energy Medicine in Therapeutics and Human Performance. New York: Elsevier; 2003.
  64. Ruden RA. A model for disrupting an encoded traumatic memory. Traumatology. 2007;13:71-75.
  65. Rubik B. The biofield hypothesis: its biophysical basis and role in medicine. J Altern Complement Med. 2002;8(6):703-717.
  66. Feinstein D. Energy psychology: a review of the preliminary evidence. Psychother Theor Res Pract Train. 2008;45(2):199-213.

Marmite – a yeast extract that modulates GABA in the brain –

An interesting study using a natural substance, Marmite, was released in April, demonstrating GABA-ergic manipulation by a nutraceutical. GABA plays a role in controlling brain activity in processes such as depression and seizures. There are no real oral sources of natural foods that can be digested and absorbed into the CNS to increase GABA levels until Marmite was found in this study. Marmite is a derivative of a yeast extract that is high in B!@ and pyridoxine (B-6) as well as glutamate. Fourteen subjects were studied in this clinical trial, each being fed a teaspoon of Marmite a day for a month with a control group being fed peanut butter. EEG demonstrated a down-regulation of evoked visual responses in the brain , the occipital lobe, which is highly GABA dependent for inhibition. It was determined that the Marmite did have an ability to decrease the visual response of the brain based on EEG, thereby was modifying the GABA control of the brain.

Dietary modulation of cortical excitation and inhibition MArmite

Using a steady-state EEG paradigm, we found that a dietary intervention had a significant effect on the brain’s response to visual stimuli, compared with consumption of a placebo. This was unlikely to be a consequence of attentional lapses, and the effects were reduced after 2 months of resuming a normal diet. These findings are consistent with an increase in the availability of GABA in visual areas of the brain that inhibits the excitability of neurons responsive to the stimulus.

This raises the possibility that dietary interventions geared towards increasing GABA concentration might reduce excitability to normal levels, and potentially alleviate some symptoms of the disorder such as seizure frequency (particularly for photosensitive epileptics). This might be of particular utility in treating patients who either do not respond to traditional medication, or who cannot take it for other reasons (e.g. pregnancy, or interactions with other drugs). The apparent involvement of GABA in other neurological and mental health conditions (Honig et al., 1988; Nemeroff, 2003; Robertson et al., 2016) suggests further potential for deployment of dietary interventions.

Of note, the vitamin content of marmite :

Vitamin B6  0.57 mg/100 g

Vitamin B12 (Cyanocobalmin)  29 mcg/100g

Glutamic Acid (Glutamate) 2.8 g/100g


Vitamin B12 enhances GABA content but reduces glutamate content in the rat suprachiasmatic nucleus



Eat your Fresh Fruit! – for better cardiovascular health: Latest New England Journal April 11, 2016

A recent study released in the April 10 edition of The New England Journal of Medicine demonstrated that fresh fruit consumption was associated with decreased blood pressure and decreased blood glucose.

Fresh Fruit Consumption and Major Cardiovascular disease in China

Increased fresh fruit consumption was associated with decreased risk of cardiovascular disease, decreased cardiovascular death, decreased coronary events, decreased hemorrhagic stroke, and decreased ischemic strokes.


Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer_ systematic review and dose-response meta-analysis of prospective cohort studies

Increased consumption of fruit and vegetables for the primary prevention of cardiovascular diseases.

Dietary Nitrate Lowers Blood Pressure

Fruit and vegetable consumption and all-cause, cancer and CVD mortality analysis of Health Survey for England data.

Fruit and Vegetable Consumption and Risk of CAD – a metanalysis of cohort studies

Quantity and variety in fruit and vegetable intake and risk of coronary heart disease

Greater Total Antioxidant Capacity from Diet and Supplements Is Associated with a Less Atherogenic Blood Profile in U.S. Adults

Novel insights of dietary polyphenols and obesity

Cruciferous vegetable consumption is associated with a reduced risk of total and Cardiovascular disease mortality

The NEJM study released in this issue death with Chinese populations, some 450,000 Chinese in fact, with no prior stroke or hypertension to avoid confounding factors. IN Western populations, an inverse association had been seen in patients eating 80 gm of fruit a day, leading to a 5% decrease in cardiovascular death.

A low level of fruit intake is associated with a major increased cardiovascular risk rate. The study above chose China, since vegetable intake is high but fresh-fruit intake is much lower.  Cardiovascular disease causes 17 million deaths a year and is especially high in lower income countries. The effect of adding fruit to the diet of people with low consumption rate can detect larger effects.


The association between the level of fruit consumption and cardiovascular risk in our study (a 40% lower risk of cardiovascular death and a 34% lower risk of major coronary events among participants who consumed fresh fruit daily as compared with those who never or rarely consumed fresh fruit) was much stronger than the associations observed in previous studies. < Current NEJM study April 2016.    This study involved some 512,000 people who had low intake of fruit already, making it easy to detect positive benefits. None of the patients had hypertension or Diabetes, and thus were not on any confounding medications. The study also took into account regression dilution bias (changes in baseline characteristics of a population during a study) that may impact findings. 

Fruit is high in fiber, potassium, folate, phytochemicals, and antioxidants all of which may mediate the positive impact of fruit intake.


In conclusion, our evaluation of the relationship between fresh fruit consumption and cardiovascular disease in China showed that the level of fruit consumption was inversely associated with blood pressure and blood glucose levels.

Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010 a systematic analysis for the Global Burden of Disease Study 2010.

Up-regulating the Human Intestinal Microbiome Using Whole Plant foods, polyphenols and fiber

Health benefits of fruit and vegetables are from additive and synergistic combinations of phytochemicals

What is Xenohormesis

White Pitaya (Hylocereus undatus) Juice attenuates insulin resistance and hepatic steatosis in obese mice

Greater Total Antioxidant Capacity from Diet and Supplements Is Associated with a Less Atherogenic Blood Profile in U.S. Adults b

Feeding the brain and nurturing the mind linking nutrition and the gut microbiota to brain development

Cultivating healthy growth and nutrition through the gut microbiota.




Eat your greens – chlorophyll metabolites in our blood may be maintaining our blood anti-oxidants.

  • Eat your greens!
    Eat your greens!

    Everyone knows about CoQ10, with many people frequently taking it for ‘vascular health’ . It is true that ubiquinol in the blood stream is an anti-oxidant that helps maintain vascular integrity. Ubiquinol–10  is an endogenously synthesized lipid antioxidant that scavenges free radicals and is involved in a-tocopherol homeostasis. It prevents lipid peroxidation and in the process is oxidized to ubiquinone.

  • 95 % of the quinone is maintained as ubiquinol, which must be regenerated from ubiquinone after it prevents lipid oxidation.
  • The study below demonstrated derivatives of chlorophyll can catalyze the reduction of ubiquinone to generate ubiquinol in plasma. The chlorophyll in our system is obtained from green leafy vegetables, and it is derivatives of the chlorophyll that may be catalyzing the reforming of ubiquinol, rather than ascorbic acid, carotenoid, tocopherol and flavonoid antioxidants that are usually given the credit for this process.
  • In the blood stream, metabolites of chlorophyll , such as chlorophyllide a, pheophytin-a, pheophorbide-a, methyl pheophorbide-a, 10-OH-pheophorbide-a, 10- OH-methyl pheophorbide-a, pyro pheophorbide-a and methyl pyropheophorbide are formed and may catalyze the photoreduction of ubiquinone to ubiquinol.
  •  Both light and light-absorbing chlorophyll metabolites can be present in capillaries, arteries and veins of several animals including humans. If chlorophyll metabolites catalyze the photoreduction of plasma ubiquinol in vivo, it would be a novel mechanism to maintain high levels of plasma ubiquinol – and this is what the paper listed in it’s research proposes, is that light through our skin drives chlorophyl metabolites to regenerate the phytonutrient ubiquinol.
  • Dietary Chlorophyll Metabolites Catalyze the Photoreduction of Plasma ubiquinone
  • Bottom line: Eat your greens and get sunshine!

Consumption of fruits and vegetables was inversely associated with stroke incidence, stroke mortality, ischemic heart disease mortality, and CVD mortality.

Known modifiable risk factors for CVD include smoking, sedentary lifestyle, diet, dyslipidemia, hypertension, obesity, and type 2 diabetes.

The observed protective effect of consuming plant foods on chronic diseases is likely due to their bioactive components.

Plant Bioactives:

  1. Phytosterols are naturally-occurring plant sterols found in the non-saponifiable fraction of plant oils. Plants synthesize several types of phytosterols (e.g., sterols and stanols) that are structurally similar to cholesterol, except for the functional group substitutions on the sterol side chain at the C24 position. Beta-sitosterol (most abundant), campesterol, and stigmasterol comprise almost our entire intake of phytosterols. Since humans do not synthesize phytosterols, they must be obtained from the diet. The main dietary sources of naturally-occurring phytosterols are vegetable oils, nuts, grains and, to a lesser extent, fruits and vegetables. Commonly consumed products that are fortified with phytosterols, such as Benecol™ and Take Control™ are found in many foods. . Benecol spread contains stanol esters derived from tall oil (pine tree wood pulp) and Take Control margarine contains sterol esters from soybeans. Consuming 2–3 g/d of phytosterols from these products resulted in approximately 14% reduction in LDL  with no change in HDL. Thus, both sterols and stanols are equally effective in lowering LDL concentration. NCEP ATP 111 guuidelines: two grams of plant sterol or stanol esters daily for optimal dietary therapy for elevated LDL.
  2. Flavonoids: The most common flavonoids are flavones, flavanols, catechins, and anthocyanins, along with anthoxanthins. There is an inverse relationship between flavonoid intake and chronic diseases including CVD. Red wines contain an abundance of polyphenols including phenolic acids (for example, gallic acid, and caffeic acid), stilbenes (resveratrol), and flavonoids (for example, catechin, epicatechin, quercetin, rutin) . Gallic acid has more antioxidant activity than caffeic acid. Wine polyphenols can induce vasorelaxation via nitric oxide synthesis , decrease platlet aggregation, and decrease inflammatory mediators. Resveratrol is a polyphenol found principally in the skin of grapes and, in lesser amounts, in peanuts. It inhibits both LDL oxidation and platelet aggregation and scavanges free radicals.
  3. Lignans: Lignans are polyphenols found in plants, especially in flaxseed (secoisolariciresinol diglucoside), sesame seeds (sesamin, sesamolin), and soy, followed by whole-grains cereals (syringaresinol), and legumes, including nuts. Fruits and vegetables contain a wide variety of lignans (e.g., matairesinol (MAT), pinoresinol (PINO) and lariciresinol (LARI)) but in minute quantities. The proposed mechanisms by which dietary lignans could reduce the risk of CVD include the phytoestrogenic, and antioxidant activity of these compounds and their metabolites. Some plant lignans such as matairesinol (MAT), secoisolariciresinol (SECO), pinoresinol (PINO), and lariciresinol (LARI) are metabolized by intestinal bacteria to enterolignans (enterodiol and enterolactone) in various proportions.
  4. Resistant starches: Complex carbohydrates derived from starch contribute over half of humans’ daily energy requirements. Starch is a homopolysaccharide made in plants and stored in granules. Amylose and amylopectin are two polymers found in starch and are identified based on the glycosidic bond linking the α-D-glucose monomers. Amylose is a linear polymer with α-(1,4) linkages while amylopectin has linear α-(1,4) linkages and α-(1,6) branch points. There are four types of resistant starches – types one to four. Dietary sources of RS 1 include partially milled grains and seeds. RS 2 can be found in raw potatoes, legumes, just-ripe bananas, and high-amylose maize (HAM). RS 3 results from retrograded foods, such as potatoes, cereals, and breads. Chemically- or physically-modified starch and resistant maltodextrins are known as RS 4 and 5, respectively.  Due to lack of enzymatic hydrolysis, the direct contribution of glucose to blood from RS is minimal and allows for an attenuated post-prandial glycemic response.  Peripheral insulin sensitivity (Si) also improved by approximately 20% in individuals with metabolic syndrome consuming the same amount or RS.  There is  production of short chain fatty acids (SCFA) from RS fermentation by gut microbiota in the large intestine which tereby makes RS bioactive. The SCFA are capable of influencing risk, and even treatment, of NCDs such as diabetes and cancer through several mechanisms: decreasing luminal pH, enhancing mineral absorption, and stimulating the release of two satiety peptides known as glucagon-like peptide -1 (GLP-1) and peptide tyrosine tyrosine (PYY) to the periphery . RS can act as a prebiotic to selectively increase the concentration and viability of certain bacteria, such as Ruminococcus bromii .Intra-individual variation in gut microbiota may influence RS fermentation, the production of SCFA, and upregulation of GLP-1.
  5. Cyclic Dipeptides: Cyclic dipeptides (also known as 2,5dioxopiperazines; 2,5-diketopiperazines; cyclo (dipeptides); or dipeptide anhydrides) are relatively simple compounds and, therefore, are among the most common peptide derivatives found in nature. Consistent with a role for fermentation process in synthesis of cyclic dipeptides is the observation of high levels of cyclo (His-Pro) in foods that undergo fermentation and/or high heat treatment of protein-rich foods. Such examples are nutritional supplements (e.g., TwoCal HN and Jevity), milk, yogurt, sauces, and fermented fish . Active cyclic dipeptides include cyclo (His-Pro), cyclo (Leu-Gly), cyclo (Tyr-Arg), and cyclo (Asp-Pro). Of these only cyclo (his-Pro)[CHP] has been shown to be endogenous to animal kingdom. CHP may act as an appetite suppressant and satiety-inducer.  There is a possible role of CHP in insulin secretion and glucose metabolism.  CHP  causes higher insulin excursions without any change in C-peptide suggesting that CHP may decrease hepatic insulin clearance.    Items with CHP include tuna, fish sauce, Dried Shrimp , Spent Brewer’s Yeast hydrolysate, and others.
  6. Fruit Berries:  Polyphenols found in berries and other plant foods are particularly associated with anti-inflammatory, antioxidant, cardioprotective, and chemopreventive properties. Several compounds contribute to the antioxidant properties of berries and are typically found in the outer parts of the fruit or berry, most often as cinnamic and/or benzoic acid derivatives. Tanins, Anthocyanins,  carotenoids and stilbenes such as resveratrol are present in berries. Some amounts of resveratrol can be found in cranberries, strawberries, and other berries. Chokeberry, bilberry, and blackcurrant berries have the highest antioxidant capacity of the different berry fruits (umol Trolox/g fresh weight), and whole fruit extracts have greater antioxidant activity than many isolated phenolic compounds or vitamins . Strawberries are known to be high in phenolic compounds such as the phenolic acid derivative ellagic acid, and contain a significant amount of vitamin C. Blueberries are noted for a wide variety of anthocyanin compounds, while both cranberries and blueberries also contain significant concentrations of phenolic acids. Anti-oxidants in  Berries provide  anti-inflammatory activity, free radical scavenging and up-regulation of antioxidant enzyme genes, decreased levels and antioxidation of LDL, increases in circulating HDL, inhibition of platelet activation and aggregation, and improvements in endothelial function. Berries have been shown to provide improvements in blood pressure or hypertensive status due to increased NO bioavailability via activation of endothelial NO synthase.

Bioactive Plant Metabolites in the Management of Non-Communicable Metabolic Diseases

Statins’ effect on plasma levels of Coenzyme Q10 and improvement in myopathy with supplementatio

Light-harvesting chlorophyll pigments enable mammalian mitochondria to capture photonic energy and produce ATP  <– we show that mammalian mitochondria can also capture light and synthesize ATP when mixed with a light-capturing metabolite of chlorophyll. To demonstrate that dietary chlorophyll metabolites can modulate ATP levels, we examined the effects of the chlorophyll metabolite pyropheophorbide-a (P-a) on ATP synthesis in isolated mouse liver mitochondria in the presence of red light (lmax5670 nm), which chlorin-type molecules such as P-a strongly absorb (Aronoff, 1950), and to which biological tissues are relatively transparent. We used P-a because it is an early metabolite of chlorophyll, however, most known metabolites of chlorophyll can be synthesized from P-a by reactions that normally take place in animal cells The same metabolite fed to the worm Caenorhabditis elegans leads to increase in ATP synthesis upon light exposure, along with an increase in life span.   Results suggest chlorophyll type molecules modulate mitochondrial ATP by catalyzing the reduction of coenzyme Q, a slow step in mitochondrial ATP synthesis. We propose that through consumption of plant chlorophyll pigments, animals, too, are able to derive energy directly from sunlight. We show that dietary metabolites of chlorophyll can enter the circulation, are present in tissues, and can be enriched in the mitochondria. When incubated with a light-capturing metabolite of chlorophyll, isolated mammalian mitochondria and animal-derived tissues, have higher concentrations of ATP when exposed to light, compared with animal tissues not mixed with the metabolite. The hypothesis is that photonic energy capture through dietary-derived metabolites may be an important means of energy regulation in animals.

  • To synthesize ATP, mitochondrial NADH reductase (complex I) and succinate reductase (complex II) extract electrons from NADH and succinate, respectively. These electrons are used to reduce mitochondrial CoQ10, resulting in ubiquinol (the reduced form of CoQ10). Ubiquinol shuttles the electrons to cytochrome c reductase (complex III), which uses the electrons to reduce cytochrome c, which shuttles the electrons to cytochrome c oxidase (complex IV), which ultimately donates the electrons to molecular oxygen. As a result of this electron flow, protons are pumped from the mitochondrial matrix into the inner membrane space, generating a trans-membrane potential used to drive the enzyme ATP-synthase.
  • Photons of red light from sunlight have been present deep inside almost every tissue in the body. Photosensitized electron transfer from excited chlorophyll-type molecules is widely hypothesized to be a primitive form of light-to-energy conversion that evolved into photosynthesis. Electrons would be transferred by a metabolite of chlorophyll to CoQ10, from a chemical oxidant present in the mitochondrial milieu. Many molecules, such as dienols, sulfhydryl compounds, ferrous compounds, NADH, NADPH and ascorbic acid, could all potentially act as electron donors. Intense red light between 600 and 700 nm has been reported to modulate biological processes. . Exposure to red light is thought to stimulate cellular energy metabolism and/or energy production by, as yet, poorly defined mechanisms. On a clear day the amount of light illuminating your brain would allow you to comfortably read a printed book. Photons between 630 and 800 nm can penetrate 25 cm through tissue and muscle of the calf . Adipose tissue is bathed in wavelengths of light that would excite chlorophyll metabolites. Utilization of these facts may have the potential for new therapies. A potential pathway for photonic energy capture is absorption by dietary-derived plant pigments. Dietary metabolites of chlorophyll can be distributed throughout the body where photon absorption may lead to an increase in ATP .

Chlorophyll-related compounds inhibit cell adhesion and inflammation in human aortic cells.

Chlorophyll Revisited Anti-inflammatory Activities of Chlorophyll a and inhibition of expression of TNFa

An Evidence Based Systematic Review of Chlorophyll by the Natural Standard Research Collaboration

An Evidence Based Systematic Review of Goji Lycium spp by the Natural Standard Research Collaboration

Risk of new-onset diabetes associated with statin use




Insane Medicine – Liraglutide (Saxenda) for weight loss!!

  • Liraglutide is a glucagon-like 1 peptide that has been available for diabetes management for a few years and now has an added FDA approval for weight loss management!!
  • There are more options for weight management as of now!
    There are more options for weight management as of now!


  • To date, Phentermine/topiramate ER (Qsymia) is the most effective drug available. Locaserin (Belviq) is another approved drug for weight loss, but it is less effective.  However, it is better tolerated. Other options such as Xenical are helpful, but it prevents absorption of food and can cause excessive bloating and gas in some patients. Contrave (Wellbutrin and Naltrexone) is also effective but has neuropsychiatric effects.
  • Liraglutide is used to treat type 2 diabetes at a dose of 1.8 mg a day. It is injectable. The weight loss form of the drug is a dose of up to 3.0 mg a day injected. The amount of weight loss varies as the dose approaches the upper limit of 3 mg a day.
  • Liraglutide decreases appetite and therefore energy intake, which is how it causes weight loss. It also delays gastric emptying. Used as an adjunct to physical exercise and dieting, it has resulted in up to an 8 kg body weight loss over the 56 week course of treatment [ −8.0±6.7% (−8.4±7.3 kg)].
  • Liraglutide treatment was associated with reductions in cardiometabolic risk factors, including waist circumference, blood pressure, and inflammatory markers. Fasting lipid profiles were also improved as well. The combination of weight loss and improved glycemic control probably contributed to the observed reductions in the prevalence of prediabetes and the delayed onset of type 2 diabetes.
  • Side effects include an increased incidence of gallstones, which commonly increase with weight loss.  Nausea and constipation (or diarrhea) has been reported. Rarely, pancreatitis and kidney failure has occurred. The FDA has required a boxed warning about the risk of thyroid C-cell tumors in the package insert, and in patient’s with a family history of Multiple Endocrine Neoplasia Type 2 or medullary thyroid carcinoma, this treatment is to be avoided.
  • Treatment is started at 0.6 mg injected a day and increased weekly by another 0.6 mg until a total of 3 mg a day is injected. At 16 weeks, if a 4% body weight loss is not achieved, therapy should be stopped. Total cost per month is about $1000.00!
  • For patients who have a BMI>30 (Body mass index) and are not diabetic, or have a BMI>27 with a risk factor, such as hyperlipidemia or diabetes, Saxenda is a consideration for weight loss.
  • Liraglutide has effects on a number of metabolic systems
    Liraglutide has effects on a number of metabolic systems

    Liraglutide has effects on a number of metabolic systems
    Liraglutide has effects on a number of metabolic systems

    Liraglutide has effects on a number of metabolic systems
    Liraglutide has effects on a number of metabolic systems

Neuroprotective and anti-apoptotic effects of liraglutide on SH-SY5Y cells exposed to methylglyoxal stress

A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management

Liraglutide (Saxenda) for Weight Loss

Insane Medicine – Akkermansia muciniphila and the Gut biome

  • The bacteria in your gut create a huge ecosystem or biome that has major effects on your overall health. More and more studies are demonstrating this, including the one below.
  • The gut microbiota diversity and function plays a role in the development of obesity and metabolic ailments.
  • Akkermansia muciniphila is a mucin-degrading bacteria found in the mucus layer of the intestine that has been found to help improve your metabolic status by increasing insulin sensitivity and glucose regulation.
  • Obese individuals and those with Type 2 diabetes differ from leaner individuals in the constitution of their gut micobiome and the microbial gene richness. It has been found in mice that higher levels of  mucin-degrading bacteria (Akkermansia muciniphila) are inversely associated with body fat and glucose intolerance. In other words, these bacteria help improve glucose metabolism and improve overall metabolic health.
  • The article below demonstrated that Akkermansia muciniphila, when increased in the gut, resulted in healthier metabolic status in obese people. This was accomplished by caloric restriction, which then resulted in increased microbial gene richness ( a good thing) and improved glucose homeostasis and blood lipids. Following a FODMAP diet also increased Akkermansia muciniphila in the gut.
  • The higher the Akkermansia muciniphila bacteria levels are in the gut, it seems that you will have better glucose metabolism, better waist-to-hip ratios, lower fasting glucose levels, better triglyceride levels,  and better fat distribution.
  • Increasing amounts of fat in the form of fat hypertrophy is a proinflammatory condition and is associated with bad cardiometabolic risk. This inflammatory risk is measured through insulin levels, interleukin-6, lipopolysaccharide levels, and C reactive protein levels in the blood stream. Caloric restriction leads to increased Akkermansia muciniphila and other healthy bacteria, which increases the overall microbial gene richness. These bacteria lower the inflammatory markers through their metabolic activity. This results in better metabolic outcomes.
  • How does this all occur? Akkermansia muciniphila ferments waste products into other items that other beneficial bacteria species can feed on. Short chained fatty acids are one of those items as well as acetate, which becomes an anorectant when absorbed in the body. In other words, you eat less.
  • The key here is that the gut biome plays a tremendous role in our overall health, and caloric restriction results in a  boosting of the healthy richness of our gut biome, which is probably a key part of overall health!

KEY study in GUT :



Dao M, Everard A, et al. Akkermansia muciniphilaand improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology. Gut.2015. 

Gut Bacteria and Food Allergies:

  • Gut bacteria also seem to play an integral role in other aspects of our health including food allergies. The presence of Clostridia in our gut appears to be protective against food allergies by causing the release of Interleukin-22 from gut cells, thereby decreasing permeability of the gut to allergens, which cause allergic reaction. Without gut permeability, the antigens cannot create an allergic immune response. Food allergies have been increasing in recent times due  to modern dietary and hygienic practices, which disturb our natural gut biome.High fat diets, antibiotics,  and formula feeding have all affected our gut bacteria, some of which protect us against food allergies. In a study, it was shown that germ-free mice and mice treated with antibiotics both reacted to peanuts, however, when clostridia was introduced, the reaction went away! This demonstrates how Clostridia decreases food allergies.  The study, “Commensal bacteria protect against food allergen sensitization,” was the source of this information.
  • Clostridia protects against Food Allergies

Insane Medicine – Acid in our bodies is a problem – Metabolic acidosis (MA)

Acid is not good
Acid is not good

acid house acid mushroom

  • Our bodies are always in a battle with too much ACID. I discussed this briefly before and am revisiting this topic again because of the metabolic impact metabolic acidosis (MA)  has on our bodies (that is, too much acid)
  • In the process of digesting meats and animal proteins, our body produces acids as well as internal processes that contribute to high acid levels. Our body uses bicarbonate and other  mechanisms to neutralize the excess acid.
  • Metabolic acidosis (MA) affects every system in our body. MA at a chronic level activates bone resorption and can increase the rick of osteoporosis. Treatment of MA can decrease this risk when it is present. Skeletal strength is impaired by MA because the body cannibalizes it’s own muscle to help neutralize the extra acid. Likewise, MA will impair insulin release and insulin receptor functioning. This results in glucose intolerance and diabetes. MA will also cause the progression of kidney failure and impair the functioning of thyroid hormones and it’s receptors.
  • We see metabolic acidosis in 1 out of 30 patients with normal  kidney function. the number affected increases as kidney function declines.
  • BMC Nephrol, 2013 Jan 9;14:4 : Use of bicarbonate to normalize MA can prevent progression of chronic kidney disease. How much bicarbonate and what type of bicarbonate is used? Sodium bicarbonate, in amounts starting at 1300 mg twice a day to get the serum bicarbonate levels to 24 mg/dl. Baking soda has 850 mg of sodium bicarbonate in a teaspoon.
  • Sodium bicarbonate intake does not worsen high blood pressure because the sodium load resulting from the sodium bicarbonate cannot be reabsorbed in the kidney through the usual NACL cotransporter.
  • The body normally excretes extra acid loads produced in the body in the form of ammonia, which is produced from glutamine (an amino acid) When metabolic acidosis is present, the body quickly runs out of glutamine from its usual sources and gets extra glutamine from muscle breakdown. The glutamine then goes to the kidney to be broken into ammonia which absorbs the extra acid.  So metabolic acidosis leads to increased muscle breakdown and weakness.
  • Diet affects the production of acid, especially with the consumption of animal proteins, which results in a lot of acid production in the body. This speeds UP the loss of kidney function in predisposed individuals. It has been shown that fruits and vegetables create little acid production in the body and a vegan diet as such decreases the rate of kidney function decline in patients with kidney failure.


Here is the summary:

  1. Treatment of metabolic acidosis, when the serum bicarbonate level is below 20 mmol/L, using sodium bicarbonate at doses of 1300 mg twice a day to increase serum bicarbonate to 24 mmol/L has positive impacts in multiple fronts as below.
  2. Increased bone density results from treatment of MA, thus decreased fractures and falling.
  3. There is better glucose control by treating MA due to better insulin sensitivity and insulin receptor responsiveness.
  4. Treatment of metabolic acidosis decreases the progression towards kidney failure in susceptible individuals with chronic kidney disease.
  5. Treatment of MA results in better muscle strength and muscle mass.
  6. Eat more fruits and vegetables to decrease your intake of acids.
  7. Have your doctor asses your blood for low bicarbonate (Less than 20 mmol/L)
  8. Consult your doctor prior to initiating any medical regimen as discussed.

Insane medicine – Replace saturated fats in your diet with Vegetable oils (Linoleic acid) to lower cardiac risk!

Replacing saturated fat with vegetable oil is associated with lower coronary artery disease risk based in a study in Circulation recently released (Circulation. 2014;130:1568-1578).

  1. Exchanging 5% of consumed calories from saturated fat sources (red meat and butter) with foods containing linoleic acid (an n-g fatty acid that is polyunsaturated and found in vegetable oil, seeds, and nuts) can decrease coronary heart disease events by 9%. So swap out your saturated fat sources with polyunsaturated fat to help out your heart!
  2. Linoleic acid (polyunsaturated fat) intake was inversely associated with heart disease, such that the more linoleic acid taken in, the lower the risk of heart disease. At the best outcomes, there was a 15% lower heart-risk and 21% lower death rates in those who consumed the most linoleic acid sources.
  3. Replace butter, lard, and fat from red meat with liquid vegetable oils when you prepare and cook foods.  By replacing saturated fat in this way, total and LDL cholesterol is reduced.
  4. Sources of Linoleic acid (an omega-6 polyunsaturated fat) include: soybean, sunflower, safflower, and corn oil, as well as nuts and seeds.
  5. Fats have 9 calories per gram. Use 1.5-3 tablespoons of vegetable oil daily to get 5-10% of calories from linoleic acid (100-200 calories total) It is important to replace saturated fat with these sources of polyunsaturated fats (linoleic acid) and not just adding this to the total fat intake.
  6. Linoleic acid does not promote inflammation based on a neutral effect on inflammatory markers or arachidonic acid levels (which increase in inflammation).

Cooking oil examples:

Safflower oil – 78 % PUFA (Linoleic acid)

Sunflower oil – 69% PUFA (Linoleic acid)

Corn oil – 62%

Soybean oil  – 61 %

Peanut Oil  – 34%

Canola oil  – 29%

Lard – 12 %

Palm oil – 10%

Olive oil  – 9%

Butterfat  – 4%

Palm kernel oil  – 2%

Coconut oil – 2%


General notes about fats:

  • Greater intake of trans-fats (hyrogenated oil for example) relative to polyunsaturated fats (PUFA) is associated with higher cardiac risk. N-3 omega fatty acids and alpha-linoleic (ALA), also an n-3 fatty acid) are associated with good cardiac risk. Linoleic acid (LA) , an n-6 PUFA most commonly eaten in the Western diets, also has been shown to be beneficial in preventing cardiac risk, but less investigation had been done regarding this fatty acid. Linoleic acid reduces LDL levels, which is a positive effect for decreasing cardiac risk. LA can be elongated into arachidonic acid, which is inflammatory and thrombogenic (blood clot forming). Studies have shown that LA is in fact not pro-inflammatory in the body. It does not increase C-reactive protein . It also has no effect on other inflammatory marker such as cytokines, fibrinogen, soluble vascular adhesion molecules, plasminogen activator inhibitor type 1, or tumor necrosis factor-α.
  • There appears to be a linear response to increasing LA intake – as one takes in more LA, there is less coronary events (heart attacks) and less death! Thus n-6 fatty acids (Linoleic acid) has cardioprotective effects! Increasing LA intake by 5% led to 9% less coronary heart disease and 13% less death!
  • It had been assumed that LA is converted to arachidonic acid (AA), which is inflammatory. AA  is the main precursor of eicosanoids with inflammatory and thrombogenic properties, such as prostaglandin E2, thromboxane A2, and leukotriene B4. It has been found, however, that the conversion of LA to AA is tightly controlled in the body, thus there is no increase in inflammation.