We love matcha tea! Here is a summary why we love it so much and drink it often.
The health benefits of green tea consumption have been reported to include: cancer inhibition, allergy relief effects, cognitive dysfunction, and preventive effects on metabolic syndrome (Fujioka et al., 2016). “In a large epidemiological study, which was based on a follow-up investigation of 82,369 Japanese people for 13 years, green tea consumption also showed positive effects such as lowering the risk of cardiovascular diseases and stroke” (Fujioka et al., 2016). Dietary polyphenols found in green have been identified as potent antioxidants. In fact, green tea polyphenols have been shown to modulate different categories of antioxidant biomarkers, such as vitamins, trace elements, and enzyme systems (Vogt & Richie, 2007). “Administration of epigallocatechin gallate (EGCG), the most abundant polyphenol in green tea, was shown to restore chemically reduced tissue levels of antioxidant vitamins A, C and E in rats” (Vogt & Richie, 2007).
Interestingly, green tea polyphenols have been shown to upregulate the endogenous synthesis of intracellular glutathione (GSH) and glutathione peroxidase, while attenuating mitochondrial oxidative stress (Basu et al., 2013). Upregulation of glutathione is a very important, since its deficiency has been implicated in aging, cardiovascular disease and cancer(Vogt & Richie, 2007). The study by Vogt & Richie observed an increase in plasma antioxidant capacity in both green tea beverage and extract groups at 8 weeks, which can be an appropriate target for people with metabolic syndrome since the scenario presents with elevated systemic oxidative stress and impaired antioxidant status.
There are two prominent methods for serving green tea. The general serving method consists of steeping the leaves in hot water and filtering them through a tea strainer. In contrast, in traditional Japanese tea ceremony, fine powdered green tea leaves (matcha) are foamed with a tea whisk in hot water. I have switched to matcha tea and also recommend it often, as I found drinking the 3-5 cups of green tea to obtain the benefits did not fit into my schedule. I also found matcha more enjobale! The consistency is very creamy with an interesting flavor. I also find the ceremony of mixing it very enjoyable.
Farmers cultivate matcha by covering their tea plants 20–30 days before harvest to avoid direct sunlight. This increases chlorophyll production, boosting the amino acid content and giving the plant a darker green color. Once the tea leaves are harvested, the stems and veins are removed and the leaves are ground up into a fine powder known as matcha.
Matcha also seems to have more potent health benefits than its steeped counterpart. Here are some of the benefits I found in research:
- Reactive oxygen species-Powder teas showed the tendency of higher inhibitory effect on ROS than the same amount of leaf teas (Fujioka et al., 2016). The powdering process increased the EGCG extraction by more than 3 times, which likely contributes to the higher antioxidant activity.
- More catechins- Matcha also has more catechins and antioxidants, as much as 137 times greater than steeped green tea (Healthline, n.d.).
- Liver protection-Matcha can significantly reduce liver enzymes as observed in studies with people with non-alcoholic fatty liver disease.
- Cognitive performance-some research indicates that match can elevate cognitive performance. Researchers found that matcha caused improvements in attention, reaction time and memory, compared to the placebo (Healthline, n.d.). This can be attributed to some of the caffeine content, but also l-theanine that is found in matcha tea, which can promote alertness and mitigate the stimulatory effects of the caffeine. I have found the “buzz” from matcha to give me an alert and calm feeling at the same time…it’s actually quite amazing.
- Cancer prevention-The higher content of EGCG can have potent anti-cancer properties, as seen in vitro studies using prostate, skin, liver and lung cancer cells (Healthline, n.d.).
- Improve lipid status-Some studies show that matcha can reduce LDL cholesterol and triglycerides, and also prevent the oxidation of LDL as well. This associates matcha tea with a reduce risk of heart disease and stroke.
- Weight loss-The constituents of green tea are associated with aiding in weight loss. Since matcha comes from the same plant as green tea and has comparable nutrient profile, it can be inferred that matcha would also aid in weight loss.
As a side note, matcha can have heavy metals and pesticides, so it is best to use organic and a brand that removes most of the contaminants. I did a bit of research and found that Teavana brand was a good brand and this is the brand we use. Matcha is great as a latte. You can use flax milk and sweeten with raw honey to make this into an enjoyable, health boosting treat!
Basu, A., Betts, N. M., Mulugeta, A., Tong, C., Newman, E., & Lyons, T. J. (2013). Green tea supplementation increases glutathione and plasma antioxidant capacity in adults with the metabolic syndrome. Nutr Res, 33(3), 180-187. doi:10.1016/j.nutres.2012.12.010
Fujioka, K., Iwamoto, T., Shima, H., Tomaru, K., Saito, H., Ohtsuka, M., . . . Manome, Y. (2016). The Powdering Process with a Set of Ceramic Mills for Green Tea Promoted Catechin Extraction and the ROS Inhibition Effect. Molecules, 21(4), 474. doi:10.3390/molecules21040474
Healthline (n.d.). 7 Evidence –Based Benefits of Matcha Tea. Retrieved (2018, February 22) from https://www.healthline.com/nutrition/7-benefits-of-matcha-tea
Adapted from Maryland University of Integrative Health
o 1 ½ pounds cauliflower, trimmed and cut into 1-inch florets
o 6 Tbsp. freshly squeezed lemon juice ( I used Lime!)
o 6 Tbsp. EVOO
o ½ tsp. ground turmeric
o ¼ tsp. ground coriander
o ¼ tsp. ground cumin
o 1/8 tsp. ground cinnamon
o Sea salt
o ¼ tsp. freshly ground pepper
o 1 cup tightly packed coarsely chopped parsley
o ½ cup coarsely chopped tightly packed mint
o 1 medium cucumber, peeled, seeded, and diced o 12 cherry tomatoes, halved (I skipped this due to food sensitivity)
Method of preparation:
Place the cauliflower florets in a steamer basket and steam until just tender-crisp, 5 to 6 minutes. Remove from the heat and let cool slightly.
Place the cooked cauliflower in the bowl of a food processor and pulse about 15 times, until the texture is fine, with pieces about the size of rice grains.
In a large bowl whisk together lemon juice, olive oil, turmeric, coriander, cumin, cinnamon, 1/2 teaspoon of salt, and pepper. Add the cauliflower and toss well to coat. Taste, and adjust with a couple of pinches of salt if needed.
When the cauliflower has completely cooled, fold in the parsley, mint, cucumber, and tomatoes. Serve at room temperature.
Notes: Cauliflower just like walnuts, visually reminds us of the brain. Nutritionally is a brain-boosting superstar, filled with B vitamins, omega-3s, phosphorus, and manganese. It helps with the liver detoxification; happy liver makes a happy brain. Cauliflower comes also in deep purple higher in anthocyanins brain boosting antioxidants and orange color has more beta carotene.
1 tbsp ghee
1 cup of white mushrooms, cleaned and cut into pieces
garlic clove, chopped into pieces or 1 tablespoon minced garlic
1 small onion 1 lb. grassfed organic beef, browned and set aside
2 cups beef broth
½ cup dairy free sour cream
gluten-free pasta, cooked according to directions (I like the gluten-free brown rice pasta from Tinkyada or lentil pasta or chick pea pasta)
salt and pepper, to taste
1–2 tbsp fresh parsley, minced
In a skillet over medium-high heat, melt ghee and add mushrooms, garlic, and onion, sauté until soft. Add the browned beef and combine. Pour in broth and sour cream. Mix gently. Add cooked gluten-free noodles, turn heat to low, and mix everything together. Add salt, pepper, and parsley as desired.
Powerful Phytochemical Rich Foods that Fight Cancer
Cancer is recognized worldwide to be a major health problem in the modern world. Cancer is a systemic disease with various causes, some of which include a poor diet, toxin exposure, nutrient deficiencies and to some extent genetics. The management of cancer can be invasive and complex, and involves conventional approaches such as surgery, radiation and chemotherapy. Despite these modern advances, cancer continues to account for fourteen million new cases and roughly eight million deaths each year (Kotecha, Takami, & Espinoza, 2016). As a result, alternative methods may be needed to improve the effectiveness of the treatments and quality of life of patients.
The good news is that certain foods are cancer fighting and can both prevent and also help in the treatment of cancer therapy! That is because foods contain phytochemicals. I like to think of them as fight-chemicals, or chemicals that help you fight disease. Phytochemicals are naturally occurring plant chemicals that play important roles in health (Murphy, Barraj, Spungen, Herman, & Randolph, 2014). For example, beta-carotene (think carrots) and lycopene (think tomatoes) can reduce the risk of cardiovascular disease (CVD). Others such as lutein and zeaxanthin may reduce the effects of oxidative damage that is associated with age related macular degeneration. And ellagic acid found in raspberries may reduce oxidative damage to DNA (Murphy et al., 2014).
Over production of free radicals and inflammation are some of the contributing factors to the development of cancer. Naturally occurring phytochemicals have been found to have a wide range of cellular effects that may be chemo-protective in the early stages of cancer. Antioxidant phytochemicals can be found in many foods and medicinal plants, and they play an important role in the prevention and treatment of chronic diseases such as cancer (Zhang et al., 2015). They can also enhance the immune system, improve elimination of cancerous cells and impact your body’s repair mechanisms aimed at suppressing tumors and inhibiting cellular growth (Kotecha et al., 2016).
Foods that prevent cancer
1. Turmeric (Curcumin)-Turmeric contains curcumin which is a polyphenol that gives turmeric its golden color and distinct aroma. Curcumin’s effects against cancer have only emerged in the last few decades (Park, Amin, Chen, & Shin, 2013). Curcumin is classified as an anti-proliferative, antioxidant and carcinogen blocking agent (Park et al., 2013). In an attempt to increase its bioavailability, several curcumin formulations have been developed such as powder, tablets, capsules, liposomal encapsulation, emulsions, and nanoparticles (Shanmugam et al., 2015). Curcumin is an excellent synergist and works well in combination with other compounds such as quercetin, bioperine, piperine, lactoferrin, and soy isoflavones (Shanmugam et al., 2015). Adding turmeric and black pepper to your onions would be a great anti-cancer synergistic side dish.
2. Blueberries-consist of anthocyanins (ACNs), a water -soluble flavonoid and a member of the flavonoid family. Anthocyanins offer rich, robust, deep, dark, and beautiful colors like blues, purples, and reds in many fruits, flowers and leaves (Fang, 2014). Anthocyanins are known for their antioxidant protection. They are also known for their anti-viral, anti-inflammatory, and anti-cancer benefits. This is accomplished by increasing scavenger hunting capabilities in cells which subsequently stimulates the Phase II detoxification system. In vitro animal studies demonstrated a reduction in oxidative stress as measured in urine (urinary 8- OHdG levels), indicating that berries may also reduce free radical-induced DNA damage in animals (Wang &Stoner, 2008).
3. Tomatoes-Tomatoes are high in a phytochemical called lycopene, which is actually a carotenoid that gives tomatoes their beautiful red color. Lycopene is one of the strongest antioxidant in nature and has both free radical scavenging properties as well as the ability to provide balance within the cell’s internal defense system (Gajowik & Dobrzynska, 2014). Epidemiological studies have shown that high intake of lycopene-containing vegetables is inversely associated with the incidence of certain types of cancer, including cancer of the digestive tract, prostate and cervix. Interestingly, a combination of vitamin E, selenium and lycopene has been shown to dramatically inhibit prostate cancer development and the increase disease free survival (Scarpa & Ninfali, 2015). A meal with tomatoes, brazil nuts and avocados may be a great way to prevent prostate cancer. Lycopene has also been shown to inhibit cell proliferation and is able to induce programmed cell death of cancer cells (Kotecha et al., 2016). Tip: dietary fats can enhance lycopene absorption and metabolism. Go ahead and add some olive oil to your tomato sauce to enhance the cancer-fighting properties of lycopene.
4. Sweet potatoes- Sweet potatoes contain beta-carotene which gives them their nice orange color. The human body converts beta-carotene into vitamin A (retinol) making beta-carotene a precursor to vitamin A, which is an essential nutrient. Beta-carotene, like lycopene, exhibits anti-oxidant properties that can protect the body from free radicals, a primary cause of aging, degeneration and cancer. Beta-carotene has also been identified in the ability to inhibit the growth of cancer stem cells in neuroblastoma (Scarpa & Ninfali, 2015). The only caveat is taking beta-carotene if you are a smoker. Studies indicate that smokers can actually have an increased risk of cancer if supplemented with beta-carotene. (Virtamo et al., 2014). These findings indicate that if you smoke heavily you should consult with your health care provider before supplementing with beta-carotene.
Foods that can treat cancer
1. Aloe Vera– Aloe Vera is an amazing mixture of more than 200 constituents, including polysaccharides, enzymes, glycoproteins, amino acids, vitamins and minerals. Aloe Vera contains polysaccharides that has been associated with immune modulation (Foster, Hunter, & Samman, 2011). These polysaccharides have been shown to act as a bridge between foreign proteins and immune cells (macrophages) in the human body, facilitating the destruction of the foreigner by the macrophage. One polysaccharide in particular is called acemannan, which can interject itself into all cell membranes which can improve the metabolism of the cell. Also, acemannan is known to have antiviral and antitumor activities through activation of immune responses. Acemannan induces your macrophages to secrete three anti-cancer compounds: interferon, tumor necrosis factor-α, and interleukins. Other immune functions of acemannan include: reducing inflammation, improve macrophage function, enhance antibody release, increase T-cell production, and improve nutrient absorption through the GI-tract.
2. Green tea catechins-Green tea is a flavanol polyphenol that is really a fancy word for antioxidant compounds in the food. Of all the antioxidant compounds found in green tea, the major constituents are the polyphenols, including phenolic acids and catechins (Du et al., 2012). ECGC is the major catechin in green tea that is known for its robust antioxidant activity. In fact, effects of green tea on chemoprevention have been attributed to its antioxidant potential. They can act on inflammatory processes by altering the recruitment of inflammatory cells from the circulation (Tangney & Rasmussen, 2013). Polyphenols in green tea can improve oxidative stress markers. Green tea’s ECGC is thought to exert their anti-oxidant power by preventing specific DNA damage by free radicals and preventing tumor formation (Kotecha et al., 2016) Green tea polyphenols have been shown to directly inhibit tumor cell growth by inducing apoptosis (programmed cell death) through multiple pathways linked in cancer development.
Hippocrates once said, “let food be thy medicine, and medicine be thy food”. One of the best ways to prevent cancer is through the diet. Check out my recipes to find some cancer fighting recipes that you can enjoy!
Du, G. J., Zhang, Z., Wen, X. D., Yu, C., Calway, T., Yuan, C. S., & Wang, C. Z. (2012). Epigallocatechin Gallate (EGCG) is the most effective cancer chemopreventive polyphenol in green tea. Nutrients, 4(11), 1679-1691. doi:10.3390/nu4111679
Foster, M., Hunter, D., & Samman, S. (2011). Evaluation of the Nutritional and Metabolic Effects of Aloe vera. In nd, I. F. F. Benzie, & S. Wachtel-Galor (Eds.), Herbal Medicine: Biomolecular and Clinical Aspects. Boca Raton (FL): CRC Press/Taylor & Francis
Gajowik, A., & Dobrzynska, M. M. (2014). Lycopene – antioxidant with radioprotective and anticancer properties. A review. Rocz Panstw Zakl Hig, 65(4), 263-271.
Kotecha, R., Takami, A., & Espinoza, J. L. (2016). Dietary phytochemicals and cancer chemoprevention: a review of the clinical evidence. Oncotarget, 7(32), 52517-52529. doi:10.18632/oncotarget.9593
Murphy, M. M., Barraj, L. M., Spungen, J. H., Herman, D. R., & Randolph, R. K. (2014). Global assessment of select phytonutrient intakes by level of fruit and vegetable consumption. Br J Nutr, 112(6), 1004-1018. doi:10.1017/s0007114514001937
Park, W., Amin, A. R., Chen, Z. G., & Shin, D. M. (2013). New perspectives of curcumin in cancer prevention. Cancer Prev Res (Phila), 6(5), 387-400. doi:10.1158/1940-6207.capr-12-0410
Scarpa, E. S., & Ninfali, P. (2015). Phytochemicals as Innovative Therapeutic Tools against Cancer Stem Cells. Int J Mol Sci, 16(7), 15727-15742. doi:10.3390/ijms160715727
Shanmugam, M. K., Rane, G., Kanchi, M. M., Arfuso, F., Chinnathambi, A., Zayed, M. E., . . . Sethi, G. (2015). The multifaceted role of curcumin in cancer prevention and treatment. Molecules, 20(2), 2728-2769. doi:10.3390/molecules20022728
Tangney, C. C., & Rasmussen, H. E. (2013). Polyphenols, inflammation, and cardiovascular disease. Curr Atheroscler Rep, 15(5), 324. doi:10.1007/s11883-013-0324-x
Virtamo, J., Taylor, P. R., Kontto, J., Mannisto, S., Utriainen, M., Weinstein, S. J., . . . Albanes, D. (2014). Effects of alpha-tocopherol and beta-carotene supplementation on cancer incidence and mortality: 18-year postintervention follow-up of the Alpha-tocopherol, Beta-carotene Cancer Prevention Study. Int J Cancer, 135(1), 178-185. doi:10.1002/ijc.28641
Zhang, Y. J., Gan, R. Y., Li, S., Zhou, Y., Li, A. N., Xu, D. P., & Li, H. B. (2015). Antioxidant Phytochemicals for the Prevention and Treatment of Chronic Diseases. Molecules, 20(12), 21138-21156. doi:10.3390/molecules201219753
Milk protein (Casein)
Milk protein hypersensitivity is thought to affect well over 40% of the population. Milk protein intolerance causes a delayed response, where it can take up to 3 days to cause symptoms. These delayed reactions to milk proteins are often tested for by measuring milk-specific IgG antibodies in blood.
Milk hypersensitivity is an IgG-mediated response (often called type III hypersensitivity reactions), and is different than an allergy which is IgE-mediated. Milk hypersensitivity in early childhood is mostly an IgE-mediated response to casein, causing immediate reactions (Anthoni, Savilahti, Rautelin, & Kolho, 2009). However, IgE reactions are often rare in adulthood. Instead, a hypersensitivity in adulthood is usually Ig-G mediated.
Many symptoms resemble irritable bowel (IBS), such as bloating, constipation, migraines, headaches, runny nose, sinusitis, fatigue, skin rashes, eczema and low mood.
Egg Protein (ovalbumin)
An egg hypersensitivity typically is associated with the egg white (albumen). This differs from an egg allergy in which involves the entire egg and is characterized by immediate allergic symptoms associated with histamine (runny nose, sneezing, watery eyes, wheezing, eczema). Egg allergies are also more common among children.
An egg hypersensitivity is characterized by gastrointestinal symptoms such as excessive gas, nausea, stomach pain, and stomach cramping. Additionally, an egg hypersensitivity can reveal itself in other symptoms such as headaches, skin problems, difficulty breathing, heart burn, joint pain, irritability and nervousness. Symptoms usually come on gradually and can be dose-dependent, and is often not life threatening.
The immune response to proteins such as egg and dairy
In normal conditions, consumed proteins, including food allergens, are completely degraded in the digestive tract to oligopeptide fragments (Gocki & Bartuzi, 2016). However, 15% of protein is often found to be incompletely digested, including a proportion of food antigens. Food antigens that were not destroyed by digestive processes (such as enzymes, bile salts, gastric pH) penetrate the intestinal epithelium of the digestive tract and reach the body’s internal environment (Gocki & Bartuzi, 2016). There are four main steps involved in the immune reaction (Gocki & Bartuzi, 2016):
- Capture of antigens by Peyer’s patch M cells, which is the microfold cell. Here there are dendritic cells, macrophages, T cells and B cells.
- Capture of antigens from the digestive tract by dendritic cell processes localized by enterocytes.
- This is where it is processed to present in an MHC molecule. The dentritic cell phagocytoses the antigen and presents a peptide of the food to CD4 T cells. CD4 binds to CD28 which evokes a TH1 response. The TH1 cell produces interferon gamma, which then initiates B cell to make IgG.
- Interferon gamma will also cause CD8 T cells specific for the food to activate macrophages to produce reactive oxygen species (contributing to oxidative stress and gut inflammation). This can contribute to production of IL-1, IL-6 and even more TNF-a (Zwickey, 2018).
- Capture of antigens by enterocytes. Food antigens can also travel between enterocytes where they can damage the integrity of the cells.
- Food antigens encounter cells of the GALT (gut-associated lymphoid tissue)
- Here, food allergens will be treated by GALT either as “innocuous antigens and induce tolerance, or as pathogens and then cause either defense reactions or excessive defensive reactions, that is hypersensitivity” (Gocki & Bartuzi, 2016).
It is also important to note that TH1 also makes TNF-alpha, which is a cytokine associated with breaking down tight junctions and leaky gut. This is also contributing to many of the symptoms associated with a hypersensitivity reaction, such as GI disturbances.
Interestingly, there is a genetic component to food hypersensitivities, making some individuals more susceptible to the loss of oral tolerance; either oral tolerance is not established or it is degraded. In fact, within the first year after birth, approximately 2.5% of infants have a cow’s milk hypersensitivity, and 80% go on to outgrow it by the time they reach five years of age. On the other hand, approximately 60% of milk allergies are mediated by immunoglobulin E (IgE) rather than by immunoglobulin G (IgG)—as is seen with hypersensitivity reactions (Sampson, 2003).
Anthoni, S., Savilahti, E., Rautelin, H., & Kolho, K. L. (2009). Milk protein IgG and IgA: the association with milk-induced gastrointestinal symptoms in adults. World J Gastroenterol, 15(39), 4915-4918.
Food Intolerances. (2014, May 6). Milk Allergy or Intolerance? Retrieved 2018, May 11 from https://www.yorktest.com/milk-allergy-or-milk-intolerance/
Gocki, J., & Bartuzi, Z. (2016). Role of immunoglobulin G antibodies in diagnosis of food allergy. Postepy Dermatol Alergol, 33(4), 253-256. doi:10.5114/ada.2016.61600
Sampson, H. A. (2003). 9. Food allergy. Journal of Allergy and Clinical Immunology, 111(2), S540-S547. doi:10.1067/mai.2003.134
Zwickey, Heather. (n.d). Immune Response to Food. [presentation] Retrieved (2018, May 11) from https://learn.muih.edu/courses/6679/modules
I don’t recommend high consumptions of coconut oil and saturated fats such as often found in ketogenic diet and here is why. Both gram positive and gram negative bacteria are present in large quantities in the intestine. Gram negative bacteria, such as E. coli, might be one of the major sources for circulating endotoxin. “It has been estimated that a single cell of Escherichia coli contains approximately 106 Lipid A or endotoxin molecules and a typical human intestinal tract could harbor approximately one gram of endotoxin” (Mani, Hollis, & Gabler, 2013) The endotoxin is the gram negative bacterial outer cell wall also known as lipopolysaccharide (LPS). Even in small quantities, LPS has the potential to elicit and inflammatory response systemically. Endotoxins are thought to enter circulation through leaky intestinal epithelium in the context of leaky gut.
In recent years accumulating research has investigated the link between dietary fat and endogenous endotoxin in relation to metabolic inflammation. Current evidence suggests that dietary fat can increase circulating endotoxin concentrations. The resulting postprandial endotoxemia leads to low-grade systemic inflammation which has been implicated in the development of several metabolic diseases such as atherosclerosis, obesity, type 2 diabetes and Alzheimer’s disease (Mani et al., 2013). It has been theorized that different types of dietary oils can differentially alter intestinal endotoxin transport. According to a few studies I read, oils rich in DHA and EPA (fish oil, cod liver oil, algae oil) can attenuate LPS transport, while oils higher in saturated fats (coconut oil, palm oil, animal fats) can increase transport.
Interestingly, canola oil and sunflower oil, although containing a high unsaturated fatty acid content, augmented plasma endoxemia by 50-75%. A majority of these studies show that consuming high saturated fat diet for a longer period results in higher gram negative bacterial populations and high fiber diets results in gram positive bacterial populations. “Furthermore, even though the mechanism is not clear, high intake of fat has been shown to cause internalization of tight junction proteins and increase in the paracellular permeability to macro molecules including endotoxin” (Mani et al., 2013). Better to increase your consumption of polyunsaturated fats such as fish oil and monounsaturated fats such olive oil. This is another reason why I do not recommend long term ketogenic diets, particularly due to the high saturated fat intake.
Mani, V., Hollis, J. H., & Gabler, N. K. (2013). Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutr Metab (Lond), 10(1), 6. doi:10.1186/1743-7075-10-6
Mani, V. (2012) Understanding intestinal lipopolysaccharide permeability and associated inflammation. Retreived (2018, July 18) from https://lib.dr.iastate.edu/etd/12788/
I often recommend quercetin to my clients that I educate on supplements that are beneficial for modulating inflammation. During my research on the benefits of quercetin, I found some interesting literature that seems promising in the therapy of bladder conditions. UTI’s are one of the most common bacterial infections of the bladder and account for almost 95% of all the visits to physicians for UTI’s (Wang et al., 2012). Patients with acute cystitis always have symptoms of dysuria and increased frequency and urgency of urination. As I have already experienced, this can seriously affect a person’s quality of life. The incidence of acute cystitis is high, and the course of acute cystitis is urgent. If acute cystitis cannot be treated promptly, it will be transformed into chronic cystitis. “It can also be transformed into cystitis glandularis, and finally into bladder cancer. It can also induce nephritis. Therefore, timely treatment of acute cystitis is necessary” (Wang et al., 2012).
Currently, acute cystitis is commonly treated by systemic application of antibiotics and anti-inflammation agents. However, only a small amount of systemically administered drugs can reach the bladder. In recent years, the anti-inflammatory effect of querctin (QU) has been well recognized, demonstrating promising clinical application. Recently, it was found that QU can be used to prevent interstitial cystitis (Wang et al., 2012). There are many quercetin containing supplements available in the market, and some of them specifically aimed to treat the bladder. One of them, Cystoprotek, contains QU and rutin with the aims of reducing bladder wall inflammation (Theoharides, Kempuraj, Vakali, & Sant, 2008). Unfortunately it was recently pulled off the market. An older product, Cysta-Q, was shown to provide symptomatic improvements in patients with IC (Katske et al., 2001). Personally, neither of these supplements did anything significant for my IC symptoms at the time I was taking them. This could be due to the inability of the active ingredients to reach the bladder.
Another product that seems promising is Perque Repair Guard. The antioxidant value is of 12 servings of fruits and vegetables. It has 1g of quercetin per tablet. And other healing ingredients such as pomegranate juice powder, OPC, magnesium, chlorophyll, turmeric, and vegetable fiber.
Interestingly, some clinicians are exploring intravesical administration. This means directly instilling the drug solution into the bladder through a urethral catheter, ensuring maximum delivery of active ingredients to the bladder (Wang et al., 2012). According to Wang et. al, the bladder is an idea organ for regional therapy because it urethra provides easy access of the therapeutic agent to the bladder (Wang et al., 2012). In addition, intravesical drug administration has other potential benefits such as avoiding the first-pass metabolism, increasing drug utilization and reducing system toxicity and side effects (Wang et al., 2012). The study conducted by Wang et. al involved encapsulating nanoparticles of water soluble QU into micelles to ensure proper absorption. The results of this study found that intravesical application of the micelles did not induce any toxicity to the bladder. Even better, intravesical administration of QU micelles efficiently reduced the inflammation of the bladder with E. coli-induced acute cystitis. Results indicated that the quercetin micelle treatment can efficiently reduce the edema and inflammatory cell infiltration of the bladder in an E. coli-induced acute cystitis model (Wang et al., 2012). The data from this study proved the hypothesis that QU had potential application in acute cystitis therapy. I am looking forward to seeing future studies in the application, as there are millions of men, women, and even children suffering from this very debilitating condition!
Katske, F., Shoskes, D. A., Sender, M., Poliakin, R., Gagliano, K., & Rajfer, J. (2001). Treatment of interstitial cystitis with a quercetin supplement. Tech Urol, 7(1), 44-46.
Theoharides, T. C., Kempuraj, D., Vakali, S., & Sant, G. R. (2008). Treatment of refractory interstitial cystitis/painful bladder syndrome with CystoProtek–an oral multi-agent natural supplement. Can J Urol, 15(6), 4410-4414.
Wang, B. L., Gao, X., Men, K., Qiu, J., Yang, B., Gou, M. L., . . . Wei, Y. Q. (2012). Treating acute cystitis with biodegradable micelle-encapsulated quercetin. Int J Nanomedicine, 7, 2239-2247. doi:10.2147/ijn.s29416
Exposure to toxins may have detrimental effects on humans and animals, even at low concentrations. Specific probiotic and bacterial strains may have properties that enable them to bind to toxins we are exposed to in our environment, such as food and water. Different strains vary in their ability to bind and detoxify, often times relying on pH, contact time, and viability on the binding capacities. Below are 3 bacterial strains and a summary of their mechanisms of action on human biochemistry regarding detoxification.
Mycotoxin Degradation – Mycotoxins are secondary metabolites produced by fungi, and are capable of producing disease and death in humans (Chlebicz & Slizewska, 2019). Humans are exposed to mycotoxins while consuming plant foods such as nuts (hazelnut, almonds, pistachios), peanuts, grains and some fruits. They are also exposed to them in the environment such as often reported in mold that is found in homes that have been water damaged. Aflatoxins are secondary metabolites of Aspergillus flavus and Aspergillus parasiticus, and it has been estimated that 4.5 billion of the world’s population is exposed to aflatoxins (Wild & Gong, 2010). The aflatoxins occur mostly in tropical regions with high humidity and temperature. They accumulate post-harvest when food commodities are stored under conditions that promote fungal growth. The naturally occurring aflatoxins are AFB1, AFB2, AFG1 and AFG2, with AFB1 the most abundant, toxic and carcinogenic, and are linked to liver cancer. “However, in agriculture, other adverse effects, including toxicity, growth and immune impairment, have been widely reported and these end points are rightly of increasing focus in studies of exposed people” (Wild & Gong, 2010).
Aflatoxin B1 (AFB1) is considered to possess the highest toxicity among various types of secondary metabolites produced by a larger number of Aspergillus spp., and classified as a Group I carcinogen for humans by the International Agency for Research on Cancer (Chlebicz & Slizewska, 2019). It has been reported that AFB1 could induce growth retardation, liver cancer, and may suppress immunity. Relevant studies indicated that AFB1was mostly metabolized by cytochrome P450 (CYP 450) enzyme systems after being absorbed in the GI tract. “Subsequently, under the action of CYP 450, including CYP1A2 and CYP 3A4, AFB1 was transformed to exo-AFB1-8,9-epoxide (AFBO), which could bind to DNA, proteins, and other critical cellular macromolecules to exert its carcinogenic effect” (Chlebicz & Slizewska, 2019).
Below are two probiotics that show promise in detoxification of mycotoxins:
- Saccharomyces cerevisiae var boulardii- (note the authors indicate that since S. cerevisiae and S. boulardii are closely similar in molecular structure, they should not be viewed as separate species taxonomically, so they have been renamed as saccharomyces cerevisiae van boulardii). Inhibition of mycotoxin absorption in the GI tract is one of the mechanisms of action of this strain. The mechanism of detoxification by yeast is due to the adhesion of mycotoxins to cell-wall components. In addition, this strain can biodegrade mycotoxins (such as AFB1) to prevent adsorption of these components inside the intestines on those who consume the food that is contaminated with the aflatoxin. As a side note, Saccharomyces cerevisiae var boulardii can also degrade phytates that are also found on many of the same foods that mycotoxins are found, and this may improve adsorption of iron, zinc, magnesium and phosphorus binding (Moslehi-Jenabian, Pedersen, & Jespersen, 2010). This could be viewed as a secondary mechanism involved in detoxification.
- L. plantarum—Lactobacillus species are also able to bind mycotoxins. Via hydrophobic interactions, they are able to bind to mostly cell wall peptidoglycans, polysaccharides and teichoic acid (Chlebicz & Slizewska, 2019). L. plantarum has demonstrated to have good AFB1binding ability in vitro. It can also “increase fecal AFB1excretion, reduce lipid peroxidation, and reverse antioxidant defense systems to alleviate AFB1 toxicity” (Chlebicz & Slizewska, 2019). L. plantarum may also play a role in the suppression of CYP1A2 and CYP3A4 expression to enhance glutathione-conjugating activity and promote detoxification (Chlebicz & Slizewska, 2019). It has been reported that some lactic acid bacteria such as L. plantarum can remove AFB1 or have protective effects against AFB1. Some relevant studies demonstrated that lactobacilli could inhibit the production of aflatoxin as well as the growth of Aspergillus spp. (Huang et al., 2017). L. plantarum also demonstrates strong free radical scavenging activities and can improve antioxidant status, protecting against the effects of AFB1. “L. plantarum might also act as a biological barrier in the intestine under normal conditions, thereby reducing the bioavailability of AFB1 ingested orally and hence avoiding its toxic effects” (Chlebicz & Slizewska, 2019). I attached a chart that demonstrates some of the mechanisms of L. plantarum on detoxification of AFB1., which includes increasing AFB1 excretion, decreasing AFB1 epoxidation catalyzed by CYP1A2 and CYP3A4, coupled with enhancing the activities of different antioxidant enzymes and GST detoxification which are connected with the NrF2 signaling pathway (Chlebicz & Slizewska, 2019).
- Bacillus subtilis– This spore forming species of bacteria had some interesting mechanisms in detoxification.
Cypermethrin belongs to a group of synthetic pyrethroid insecticides which widely used in agriculture, forestry, horticulture, public health and households for the protection of textiles and to check pest infestation (Gangola, Sharma, Bhatt, Khati, & Chaudhary, 2018). . Cypermethrin is also constitute common ingredients of household insecticides (Gangola et al., 2018). Cypermethrin is an environment pollutant because of its widespread use and toxicity. Persistence may lead to serious damage to non-target organisms and various ecosystem (Gangola et al., 2018). Metabolism of cypermethrin is important because cypermethrin possess antimicrobial activities hence it prevents the beneficial microflora.
The mechanism of action is the laccase enzyme that can degrade the pesticide. Bacillus subtilis strain demonstrated to completely metabolize cypermethrin in just 15 days under laboratory conditions. The bacterial isolate harbors the metabolic pathway for the detoxification of the cypermethrin. It can also completely degrades cypermethrin without leaving any persistent or toxic metabolite (Gangola et al., 2018).
Heavy metals (Syed & Chinthala, 2015)
It is estimated that over one billion human beings are currently exposed to elevated concentrations of toxic metals and metalloids in the environment. It is also estimated that several million people may be suffering from subclinical metal poisoning. “In addition, adverse effect of heavy metals includes suppression of the immune system and carcinogenicity, neurotoxicity, mainly in children, and inhibition of the activity of some critical enzymes related to synthesis of vital biomolecules along with accumulation in the body of different organisms causing biomagnifications” (Syed & Chinthala, 2015). B. subtilis has greater ability to bind metals than Gram-negative ones due to their different cell wall structures (Cai et al., 2018). Interestingly, bacterial isolates of B. subtilis showed significant biosorption of lead. Heavy metal biosorption is the ability of bacterial cells or components to adsorb, chelate, or precipitate metal ions in the solution into insoluble particles or aggregates which can be removed either by sedimentation or filtration from the solution. Lead biosorption modifies groups like carboxyl, hydroxyl, and amino where other metal ions cannot compete offering it more affinity. The main agents in the uptake of heavy metals by B. subtilis are carboxyl groups, the sources of which are the teichoic acids associated with the peptidoglycan layers of the cell wall (Cai et al., 2018).
Cai, Y., Li, X., Liu, D., Xu, C., Ai, Y., Sun, X., . . . Yu, H. (2018). A Novel Pb-Resistant Bacillus subtilis Bacterium Isolate for Co-Biosorption of Hazardous Sb(III) and Pb(II): Thermodynamics and Application Strategy. Int J Environ Res Public Health, 15(4). doi:10.3390/ijerph15040702
Chlebicz, A., & Slizewska, K. (2019). In Vitro Detoxification of Aflatoxin B1, Deoxynivalenol, Fumonisins, T-2 Toxin and Zearalenone by Probiotic Bacteria from Genus Lactobacillus and Saccharomyces cerevisiae Yeast. Probiotics Antimicrob Proteins. doi:10.1007/s12602-018-9512-x
Gangola, S., Sharma, A., Bhatt, P., Khati, P., & Chaudhary, P. (2018). Presence of esterase and laccase in Bacillus subtilis facilitates biodegradation and detoxification of cypermethrin. Sci Rep, 8(1), 12755. doi:10.1038/s41598-018-31082-5
Huang, L., Duan, C., Zhao, Y., Gao, L., Niu, C., Xu, J., & Li, S. (2017). Reduction of Aflatoxin B1 Toxicity by Lactobacillus plantarum C88: A Potential Probiotic Strain Isolated from Chinese Traditional Fermented Food “Tofu”. PLoS ONE, 12(1), e0170109. doi:10.1371/journal.pone.0170109
Moslehi-Jenabian, S., Pedersen, L. L., & Jespersen, L. (2010). Beneficial effects of probiotic and food borne yeasts on human health. Nutrients, 2(4), 449-473. doi:10.3390/nu2040449
Syed, S., & Chinthala, P. (2015). Heavy Metal Detoxification by Different Bacillus Species Isolated from Solar Salterns. Scientifica (Cairo), 2015, 319760. doi:10.1155/2015/319760
Wild, C. P., & Gong, Y. Y. (2010). Mycotoxins and human disease: a largely ignored global health issue. Carcinogenesis, 31(1), 71-82. doi:10.1093/carcin/bgp264
I was looking for something different eat that is quick, healthy, hypoallergenic and has all the nutrients my body needs to be healthy.
So I pulled out my famous pumpkin banana muffins. This is delicious with a spoon of pumpkin seed butter and a glass of coconut water.
Full of potassium, zinc, protein omega-3 fats, you really can’t go wrong with these delicious muffins.
Side note- I have reintroduced eggs in my diet and see to tolerate them well! But if you do not tolerate eggs, you can always swap out for egg substitute powder as well!
Prep time: 15 minutes
Bake time: 30 minutes
Bake Temperature: 350F
3/4c flaxseed meal
2 eggs, beaten
2 bananas, mashed
1 scoop pumpkin seed poweder
2 tbsp pumpkin seed butter
1/2c unsweetened applesauce
1 tsp baking soda
1 tsp vanilla extract
1/4 nondairy milk
Instructions: First mix the wet ingredients. Typically, I take the bananas, vanilla extract, milk, and eggs and throw it in my Blendtech blender.
The I also mix the dry ingredients in a separate bowl. I fold the wet ingredients into the dry ingredients. You can use an electric mixer if you wish, but it really is not necessary. The batter may appear a bit dry , but that is OK. You do not want it to be too moist, it will fall apart.
You can spoon the mixture into a 12 muffin tin (using paper or greasing it with a light spray of grapeseed or avocado oil), and then form then with your hands to make then shape you desire.
Bake it for 30 minutes or until you can remove a toothpick from the center clean.
Allow to cool. Store in refrigerator.
I usually eat one for breakfast with 1 tbsp of pumpkin seed butter. High in minerals, protein, fiber and omega-3 fats, this is a delicious superfood and a quick breakfast or mid-day snack. And with the protein and fiber, this will not only provide satiety, but also help manage your blood sugar.
For this review, I want to summarize the findings on the dietary carbohydrate to protein ratio and how it may influence body composition and blood lipid profiles in adult women.
There is evidence that older adults experience age-related changes in body composition, such as increase in body fat and decrease in lean body mass (Kim, O’Connor, Sands, Slebodnik, & Campbell, 2016). A moderate energy restricted diet is often an effective way for overweight adults to reduce bodyfat mass, and improve their health profile, but it often comes with the price of a loss of 25% of body mass being lost as lean body mass (Kim et al., 2016). Accumulating data suggests that increased protein content of the diet, in combination with exercise training, can reduce the loss of lean body mass in overweight and obese subjects following a weight loss diet. This preservation of lean body mass has been attributed to the increased level of essential amino acids, especially leucine, provided by the protein (Mettler, Mitchell, & Tipton, 2010).
Current dietary guidelines recommend a daily macro-nutrient intake of 55% carbohydrate, 30% protein and 15% fat (Layman et al., 2003). However, this balance has been challenged by evidence from epidemiological, clinical and experimental studies, reporting that a higher carbohydrate intake can reduce oxidation of body fat and increase blood triglycerides (Layman et al., 2003). In particular, the optimal ratio of carbohydrate to protein has been challenged on the basis of glucose homeostasis in the context of body mass reduction. Under a higher carbohydrate intake, the body has to rely on insulin to metabolize and dispose large quantities of dietary glucose, whereas under lower carbohydrate intakes (<200g per day), the body would rely more on hepatic production to maintain blood glucose via gluconeogenesis or glycogenolysis (Layman et al., 2003).
A study conducted in 2003 by Layman et al (2003), compared the results of a moderate protein and lower carbohydrate intake to a higher carbohydrate with lower protein intake, and the influence on body mass and blood lipids. In this study, the total energy intake, fat and fiber were consistent among the two groups: 1700 kcal/day, total fat intake was 50g/day and total fiber at 20g per day. In the higher protein group (Protein Group) protein intake averaged 125g/day with a carbohydrate intake of 171g/day. The higher carbohydrate group (CHO) consisted of 68g pf protein per day and 239g of carbohydrates. The relative proportions of energy in the Protein Group were 30% protein, 41% carbohydrate and 29% fat with a ratio of carbohydrate to protein (CHO/protein) of 1.4. The proportion in the CHO Group was 16% protein, 58% carbohydrate and 26% fat with a ratio of 3.5 (Layman et al., 2003). Obviously, the cholesterol and saturated fatty acid intake was higher in the Protein group than the CHO group.
The study duration was 10 weeks. The results of the study indicated the following:
- There was not a big change in body weight between the two groups. The Protein Group lost a total weight of 7.53kg and the CHO group lost 6.96kg.
- Changes in body composition indicate the weight loss was mostly bodyfat. The Protein group lost 14.4% of initial body fat, the CHO group lost 12.2% of initial bodyfat. Loss of lean body mass tended to be greater in the CHO Group compared to the Protein Group. When changes in body composition were expressed as a ratio of fat/lean loss, the Protein group achieved a fat/lean loss of 6.36 vs. 3.92 in the CHO group. The higher protein group clearly had a stronger improvement in body composition.
- There were some differences seen in thyroid hormones, blood lipids and fasting and postprandial glucose and insulin levels, but it was not explained in detail as it was not the main objective of this study.
In summary, the results of this study indicate that the positive changes in body composition associated with the higher protein diet may be associated with either targeting of body fat or sparing of muscle protein, or both. For the purposes of improving body composition, a higher protein diet may be effective for adults.
Before I end this summary, I do want to mention I did stumble upon an interesting study in 2016 that indicates that a high protein intake eliminates the weight loss induced improvement of insulin action on postmenopausal women (Smith et al., 2016). This study indicates that a high protein diet can have adverse effects on postprandial insulin sensitivity. According to the authors, “the beneficial effect of 10% weight loss on muscle insulin action (assessed as glucose disposal rate and phosphorylation of AKT in muscle during a HECP) was eliminated by high protein (HP) intake” (Smith et al., 2016). The failure to improve muscle insulin sensitivity in the higher protein group is clinically important, because it reflects a failure to improve a major mechanism involved in the development of T2D. It also indicates more insulin is required in the higher protein group to dispose of a given amount of glucose. This can be due to:
- BCAA’s, particularly leucine, that can impair insulin mediated uptake of glucose through a negative feedback inhibition
- There may be an association of glycine and tryptophan and metabolites of acylcarnitine in the development of insulin resistance, regardless of the amount of circulating amino acid metabolites measured in the serum.
- There may be a metabolic process related to oxidative stress that is expressed in the higher protein group, as evidenced by gene expression of GSTA4 and PRDX3 that are both associated with oxidative stress. These results suggest that the adverse effect of high protein intake on insulin action during weight loss therapy may have been mediated through its effects on oxidative stress because it prevented the WL-induced decrease, and even increased, metabolic pathways involved in oxidative stress response in muscle.
- Both groups had improved liver insulin sensitivity, but the higher protein group experienced a reduction in muscle insulin sensitivity. This is attributed to the fact that protein is a potent insulin secretagogue, which may overcome the adverse effect of protein on insulin sensitivity by increasing the secretion of insulin (Smith et al., 2016).
I must mention however, protein causes greater satiation and has a greater thermogenic effect of feeding than carbohydrate and fat. This alone can lead to greater weight loss with a higher protein than a standard protein diet. “Therefore, the adverse effect of dietary protein on muscle insulin action could be offset by its effect on hepatic insulin sensitivity, insulin secretion and energy balance” (Smith et al., 2016).
In summary, this review demonstrates that the protein content of a weight loss diet can have significant effects on metabolic function and weight loss outcome. I personally believe that diets should be personalized for the individual. A high protein diet is not suitable for everyone. Neither is a high carbohydrate diet. The individual’s needs should be taken into consideration, along with various markers of health that can be measured in a blood chemistry panel, their nutritional needs (such as macronutrient deficiencies) and even nutrigenomics, health predispositions and family history. The one size fits all approach is not appropriate when prescribing nutrition therapy, as the results of these studies also demonstrate.
What do I think? The evidence is good for a higher protein diet, but I wonder if they looked into the glucogenic amino acids and their effect on insulin sensitivity. In my review, I found another journal that indeed indicated that various amino acids can actually decrease insulin sensitivity. Interestingly, it was leucine that was contributing to this change in muscle insulin sensitivity, and that is actually a ketogenic amino acid! If I find the free time at some point, I would love to research the effects of glucogenic and ketogenic amino acids and how they affect insulin sensitivity and type 2 diabetes. I personally have not been a fan of high protein diets. I feel it is too hard on the kidneys, and considering glycine is often a problem with oxalate metabolism, especially in the context B1 deficiency, I feel the risk of kidney stones is too great to recommend high protein across the board (See image). I prefer a more balance approach, with a balance of macronutrients and incorporating intermittent fasting as a way to improve blood lipids and insulin sensitivity.
Kim, J. E., O’Connor, L. E., Sands, L. P., Slebodnik, M. B., & Campbell, W. W. (2016). Effects of dietary protein intake on body composition changes after weight loss in older adults: a systematic review and meta-analysis. Nutr Rev, 74(3), 210-224. doi:10.1093/nutrit/nuv065
Layman, D. K., Boileau, R. A., Erickson, D. J., Painter, J. E., Shiue, H., Sather, C., & Christou, D. D. (2003). A Reduced Ratio of Dietary Carbohydrate to Protein Improves Body Composition and Blood Lipid Profiles during Weight Loss in Adult Women. J Nutr, 133(2), 411-417. doi:10.1093/jn/133.2.411
Mettler, S., Mitchell, N., & Tipton, K. D. (2010). Increased protein intake reduces lean body mass loss during weight loss in athletes. Med Sci Sports Exerc, 42(2), 326-337. doi:10.1249/MSS.0b013e3181b2ef8e
Smith, G. I., Yoshino, J., Kelly, S. C., Reeds, D. N., Okunade, A., Patterson, B. W., . . . Mittendorfer, B. (2016). High-Protein Intake during Weight Loss Therapy Eliminates the Weight-Loss-Induced Improvement in Insulin Action in Obese Postmenopausal Women. Cell Rep, 17(3), 849-861. doi:10.1016/j.celrep.2016.09.047