What does it mean to have a ‘healthy gut?’

Healthy gut

Can you improve the health of your gut?

The phrase ‘healthy gut’ is used a lot in the health space at the moment. But what does this actually mean? And can you improve the health of your gut? I will address these questions in the following article.

First of all, let’s define some terminology. The gut refers to the human gastrointestinal tract or GI tract. This is composed of the stomach, the small intestines and the large intestines or colon.

You may have heard the term ‘gut microbiome’ when gut health is being discussed. The human GI tract is home to 1013-1014 microorganisms or microbes (that is between 100 000 000 000 000 – 1000 000 000 000 000). In fact there are over 10 times more bacterial cells in your gut than there are your own cells making up your body. The community of microbes living in your gut is referred to as the gut microbiota. The gut microbiota is mostly made up of bacteria, but viruses and fungi are also present. The total genome content of these microbes, meaning all of the genes carried by all of these microorganisms, is referred to as the gut microbiome. Thanks to advances in the ability to sequence DNA, scientists are now starting to understand just how important this complex community of microbes is to human health and disease.

Health benefits provided by the gut microbiota

The health benefits provided by the gut microbiota include preventing disease causing bacteria, breaking down toxic compounds, shaping the immune system (1), providing nutrients, the synthesis of vitamins, particularly vitamin B and K (2) and the production of important metabolites. Metabolites are the intermediates or end products of metabolism. The metabolites produced by the microbes in the gut make up one third of all the metabolites found in the human blood and these compounds have some very important functions. Short-chain fatty acids are the main metabolic end products produced by the gut microbiota.

What are short-chain fatty acids (SCFAs)?

The main end products produced from the fermentation of undigested carbohydrates by the microbes of the colon are the short-chain fatty acids (SCFAs) acetate, propionate and butyrate (3). Fermentation is a metabolic process that converts sugars to acids, gases or alcohol that often occurs when oxygen is lacking, known as an anaerobic environment.

One of the health effects of SCFAs in the human gut is lowering the pH making a more acidic environment. This stops the growth of disease causing bacteria and increases the absorption of some nutrients (3).

Another important function of SCFAs is maintaining the gut barrier function. Don’t worry – I will explain what this means. The gut barrier is a layer of cells lining the inside of the GI tract. This layer of cells, referred to as the intestinal epithelial cells, has two jobs: controlling the absorption of nutrients, electrolytes and water from the inside of the gut into the blood stream and preventing harmful substances, such as disease causing bacteria and toxins, entering the blood stream. The mucus produced by this layer of cells also helps maintain this barrier (4). SCFAs play a role in gut barrier function by providing a fuel source for the intestinal epithelial cells thereby increasing mucus production.

The cells of our colon, known as colonocytes, also use the SCFA butyrate as an energy source (5). The SCFAs that are not used by the colonocytes travel to the liver and will be used in gluconeogenesis (a metabolic pathway that produces glucose from non-carbohydrate substances) and lipid (fat) synthesis. So SCFAs provide an energy source for the human host.

SCFAs can even act as signalling molecules in the gut where they can influence appetite by changing the production of particular hormones. A study in 2003 showed that SCFAs can activate free fatty acid receptor (FFAR) 2 and 3 (6). These receptors are found on cells in the colon that secrete the appetite suppressing hormones peptide tyrosine tyrosine (PYY) and glucagon-like peptide (GLP)-1. Studies in rabbits and rats have shown that SFCAs increase the production of PYY and GLP-1 (7, 8). A recent study using human volunteers showed that the SCFA propionate, when delivered to the colon, increased the release of PYY and GLP-1 and prevented weight gain over a 24-week period (9). While there is still a lot more research needed in this area, these results suggest that the right combination of gut bacteria producing the right amounts of SCFAs could prevent obesity.

Diseases/conditions associated with disruptions to the gut microbiota

A major change in the gut microbial community is known as dysbiosis. Dysbiosis has been linked to a number of diseases and conditions in humans including the following:

Obesity and metabolic disorder

Obesity and the associated metabolic diseases, such as type 2 diabetes, were thought to be a result of a combination of genetics and life-style factors. It now seems that the gut microbiota is also playing a role. Studies in mice have shown evidence that the gut microbiota can influence obesity. Transfer of the microbiota from obese mice to mice with no microbiota caused weight gain and insulin resistance. This did not happen when the microbiota from lean mice were transferred to mice with no microbiota (10).

Inflammatory bowel disease and Irritable bowel syndrome

Major changes in the composition and the diversity of the gut microbiota have been found in patients with inflammatory bowel diseases (11). Currently it is thought that low levels of SCFAs, particularly butyrate, are causing the inflammation that is associated with inflammatory bowel disease (12).

Problems with the composition of the gut microbiota have also been found in patients with irritable bowel syndrome (IBS). IBS is different from inflammatory bowel disease as in this disorder there is no inflammation of the lining of the intestines and the symptoms are abdominal pain, diarrhea and/or constipation. Again it is thought that low levels of butyrate are involved, as well as increases in the gas hydrogen sulfide in the gut (13).

Mood and neurological disorders

Would you believe that the microbes in your gut can change your mood and your brain function? Dysbiosis has been linked to a range of mental illnesses including autism (14), stress (15), anxiety (16) and depression (17). How is this possible? The gut microbiota are able to influence the enteric nervous system (ENS) (18). The ENS is basically the brain of the gut and controls intestinal motility and sends signals to the central nervous system (CNS). The communication that occurs between the gut microbiota, the ENS and the CNS is referred to as the microbiota-gut-brain-axis.

One way that the gut microbiota can influence the ENS is through the production of neurotransmitters. Studies in mice have shown that bacteria found in the gut can affect the metabolism of tryptophan (19), an amino acid which is required for the synthesis of the neurotransmitter serotonin. Certain bacteria from the gut of mice and humans are even able to directly make serotonin (20). Serotonin has many effects in the body, including regulating mood, perception, fear, anger and appetite, so this suggests that our gut microbiota can directly influence our behaviour in a major way!

Also, chronic stress can disrupt the intestinal barrier. This disruption is known as ‘leaky gut’. When leaky gut occurs, parts of the outer protective layer of the bacterial cell, known as the cell wall, can leak into the blood stream and cause inflammatory responses. A study from 2012 showed that the leaking of bacterial cell wall components into the blood stream may play a role in causing chronic depression in people (21).

But it is not clear whether changes in the gut microbiota can cause neurological disorders OR if neurological disorders cause changes in the gut microbiota.

What makes up a healthy gut microbiota?

The human gut contains over 1 000 different bacterial species (22). It is not yet known which combinations of microbes make up the ideal ‘healthy gut’. However, high levels of diversity are thought to be important for a healthy, well-functioning gut microbial community (23) and several diseases of the human GI tract are associated with a reduction in microbial and genetic diversity (24). A diverse gut microbiota is necessary to ensure that we extract all of the nutrients out of our diet. Humans only produce less than 20 enzymes for the digestion of complex carbohydrates. Therefore, we rely on the microbiota in the digestive tract to break down the complex carbohydrate structures found in fruits and vegetables (25).

Interestingly, major differences in the gut microbiome between Westerners and members of hunter-gatherer tribes have been observed. For example, the gut microbiota from the Hadza hunter-gatherer tribe from Tanzania is more diverse compared to urban living adults from Italy (26). The Hadza are one of the last remaining hunting-gathering communities in the world and live on a diet of wild foods including meat, honey, baobab (a fruit high in dietary fibre, vitamin C and polyphenols found in sub-Saharan Africa (27)), berries and tubers. One study has shown that a loss of diversity in the gut microbiota can result from a low fibre diet, such as a typical Western diet (28). The decrease in gut microbial diversity resulting from a typical Western diet could be a reason for the high rates of obesity and metabolic disorder in today’s population.

How can you maintain a healthy gut microbiota?

A number of factors can affect your gut microbiota including antibiotics, inflammation, ageing, GI tract motility and even the way you are born. However, it appears that diet has the greatest influence on the composition of the gut microbiota. So what can you include in your diet to promote a healthy gut microbiota?

One thing that stands out from the studies on diet and the gut microbiota is the influence of dietary fibre. Dietary fibre, particularly fibre that is classified as a prebiotic (29), appears to be important in maintaining a healthy and diverse gut microbiota (30). Prebiotics are defined as a selectively fermented ingredient that results in specific changes in the composition and/or activity of the gastrointestinal microbiota, thus conferring benefit(s) upon host health.

Finally, there is a method that is receiving attention at the moment that may gross you out, but is interesting. I am talking about feacal microbiota transplantation (FMT). Basically this means implanting the poop from a healthy person into the stomach, small intestine or large intestine of a sick person. FMT has been used successfully to treat infections with Clostridium difficile, which you may have heard referred to as C. diff. C. diff. is a nasty species of bacteria that causes severe diarrhea (31).

In the future, once we know more about what makes up the ideal healthy gut microbiota, ‘cocktails’ of beneficial bacteria may be a common method of treatment for a number of diseases and health conditions. But until then eating a diet rich in dietary fibre can help maintain a healthy gut.

  1. Ivanov, II, et al. (2008) Specific microbiota direct the differentiation of IL-17-producing T-helper cells in the mucosa of the small intestine. Cell host & microbe 4(4):337-349.
  2. Hill MJ (1997) Intestinal flora and endogenous vitamin synthesis. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation 6 Suppl 1:S43-45.
  3. Macfarlane GT & Macfarlane S (2012) Bacteria, colonic fermentation, and gastrointestinal health. Journal of AOAC International 95(1):50-60.
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  5. Pryde SE, Duncan SH, Hold GL, Stewart CS, & Flint HJ (2002) The microbiology of butyrate formation in the human colon. FEMS microbiology letters 217(2):133-139.
  6. Brown AJ, et al. (2003) The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. The Journal of biological chemistry 278(13):11312-11319.
  7. Psichas A, et al. (2015) The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. International journal of obesity 39(3):424-429.
  8. Longo WE, et al. (1991) Short-chain fatty acid release of peptide YY in the isolated rabbit distal colon. Scandinavian journal of gastroenterology 26(4):442-448.
  9. Chambers ES, et al. (2015) Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut 64(11):1744-1754.
  10. Turnbaugh PJ, et al. (2006) An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444(7122):1027-1031.
  11. Damman CJ, Miller SI, Surawicz CM, & Zisman TL (2012) The microbiome and inflammatory bowel disease: is there a therapeutic role for fecal microbiota transplantation? The American journal of gastroenterology 107(10):1452-1459.
  12. Tedelind S, Westberg F, Kjerrulf M, & Vidal A (2007) Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: a study with relevance to inflammatory bowel disease. World journal of gastroenterology 13(20):2826-2832.
  13. Matsunami M, et al. (2009) Luminal hydrogen sulfide plays a pronociceptive role in mouse colon. Gut 58(6):751-761.
  14. Kang DW, et al. (2013) Reduced incidence of Prevotella and other fermenters in intestinal microflora of autistic children. PloS one 8(7):e68322.
  15. Bailey MT, et al. (2011) Exposure to a social stressor alters the structure of the intestinal microbiota: implications for stressor-induced immunomodulation. Brain, behavior, and immunity 25(3):397-407.
  16. Bercik P, et al. (2010) Chronic gastrointestinal inflammation induces anxiety-like behavior and alters central nervous system biochemistry in mice. Gastroenterology 139(6):2102-2112 e2101.
  17. Jiang H, et al. (2015) Altered fecal microbiota composition in patients with major depressive disorder. Brain, behavior, and immunity 48:186-194.
  18. Hyland NP & Cryan JF (2016) Microbe-host interactions: Influence of the gut microbiota on the enteric nervous system. Developmental biology.
  19. Wikoff WR, et al. (2009) Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proceedings of the National Academy of Sciences of the United States of America 106(10):3698-3703.
  20. Yano JM, et al. (2015) Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell 161(2):264-276.
  21. Maes M, Kubera M, Leunis JC, & Berk M (2012) Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut. Journal of affective disorders 141(1):55-62.
  22. Rajilic-Stojanovic M & de Vos WM (2014) The first 1000 cultured species of the human gastrointestinal microbiota. FEMS microbiology reviews 38(5):996-1047.
  23. Costello EK, Stagaman K, Dethlefsen L, Bohannan BJ, & Relman DA (2012) The application of ecological theory toward an understanding of the human microbiome. Science 336(6086):1255-1262.
  24. Walker AW & Lawley TD (2013) Therapeutic modulation of intestinal dysbiosis. Pharmacol Res 69(1):75-86.
  25. Cantarel BL, Lombard V, & Henrissat B (2012) Complex carbohydrate utilization by the healthy human microbiome. PloS one 7(6):e28742.
  26. Schnorr SL, et al. (2014) Gut microbiome of the Hadza hunter-gatherers. Nature communications 5:3654.
  27. Coe SA, Clegg M, Armengol M, & Ryan L (2013) The polyphenol-rich baobab fruit (Adansonia digitata L.) reduces starch digestion and glycemic response in humans. Nutrition research 33(11):888-896.
  28. Sonnenburg ED, et al. (2016) Diet-induced extinctions in the gut microbiota compound over generations. Nature 529(7585):212-215.
  29. Gibson GR & Glenn R (2010) Dietary prebiotics: current status and new definition. Food Sci Technol Bull Funct Foods 7:1-19.
  30. Simpson HL & Campbell BJ (2015) Review article: dietary fibre-microbiota interactions. Alimentary pharmacology & therapeutics 42(2):158-179.
  31. Borgia G, Maraolo AE, Foggia M, Buonomo AR, & Gentile I (2015) Fecal microbiota transplantation for Clostridium difficile infection: back to the future. Expert opinion on biological therapy 15(7):1001-1014.

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Is açaí really so healthy?

AcaiBowlI’ll admit that I enjoy the occasional açaí bowl – and not just to look trendy. I find them very tasty and refreshing, and with such a vibrant colour I assumed they must contain some compounds that have health benefits. However, I am always dubious of so-called ‘superfoods’. The scientist in me had to dig deeper into this açaí phenomenon that has swept over all the cafés in my local area. I wanted to know if it was actually worth spending $12.50 on a small bowl of blended purple mush with some chopped fruit and coconut on top. So I went to the scientific literature and had a look at the actual studies that have been conducted on açaí.

What is açaí?

Firstly, what exactly is açaí? Açaí, or Euterpe oleracea Martius to be precise, is a slender, multi-stemmed palm plant that can reach over 30 meters. It is widely distributed in northern South America and is particularly abundant and important in the flood plains of the Brazilian Amazonian state of Pará (1). Each palm tree produces 3 to 4 bunches of berry-like fruit, each bunch having from 3 to 6kg of fruit. These round-shaped fruit start as green clusters but ripen to a dark, purple-coloured fruit that ranges from 1 – 1.5cm in diameter. The seed makes up most of the fruit, which is covered by thin fibrous fibers. There is a small edible layer under these fibres. Only 17% of the fruit is edible. Açaí berries are not eaten fresh. A juice can be made by crushing the edible pulp. This is known as açaí pulp. It is very perishable and must be frozen for export.

OK, now that we are clear on what açaí is let me tell you what I found in the scientific literature. There has been 186 studies published on açaí. One of the first studies was in 2004 published in the Journal of Agricultural and Food Chemistry. This study analysed the anthocyanin and polyphenolic compounds in açaí and the contribution these compounds have to its antioxidant capacity. It was shown that açaí pulp had a high antioxidant content compared to other anthocyanin-rich fruits such as blueberries, strawberries, raspberries and blackberries. In fact, açaí pulp had 10 times the antioxidant content of blueberries and double the antioxidant content of raspberries (2). Why is this beneficial for your health? Briefly, the production of reactive oxygen species or free radicals have been implicated in contributing to a number of chronic diseases, such as Alzheimer’s disease, cardiovascular disease and diabetes. The brain is particularly sensitive to reactive oxygen species. Dietary antioxidants, such as polyphenols, may help prevent these diseases.

A complete nutrient analysis of freeze-dried açaí found that it contains saturated and unsaturated fatty acids (32.5%), amino acids (7.6%) and sterols. Plant sterols are compounds that have been shown to lower LDL-cholesterol. Açaí is actually quite high in calories due to the presence of the fatty acids and is a complete meal containing fats, proteins and a small amount of carbohydrates (3).

Açaí is also a good source of potassium, magnesium, calcium, phosphorus, sodium and vitamins E and B1 (3). In addition, freeze-dried açaí was shown to have the highest reported antioxidant activity against the peroxyl radical (a reactive oxygen species) out of any food (4).

Another set of compounds, known as lignans, have been identified in açaí (5). The lignans from açaí contribute to the antioxidant activity of this fruit. The lignans from açaí were shown to kill human cancer cells – but remember this was done in the laboratory and not in actual human subjects (6).

Human studies involving açaí consumption

Studies conducted in animals have shown potential positive health benefits from the consumption of açaí including improvements in cholesterol levels of hypercholesteremic rats (7) and rabbits (8), protection against the characteristics of metabolic syndrome in mice (9) and a reduction of colon cancer in rats (10). Cell-based assays have found that açaí can protect human red blood cells and white blood cells from oxidative damage (11), reduce oxidative damage and inflammation in brain cells (12) and has an anti-inflammatory effect on mouse immune cells (13, 14). However, there have been very few clinical trials involving human subjects consuming açaí.

A study from 2008 found that the levels of serum antioxidants increased in human subjects 1 hour and 2 hours after they drank a juice blend containing mostly açaí when compared to subjects drinking a placebo (11). A study from the same year showed that anthocyanin concentrations in plasma increased after human subjects consumed açaí pulp or juice (15) (remember anthocyanins are one of the major antioxidants in açaí). Anthocyanins levels peaked at two hours and were higher after consuming açaí pulp compared to juice. This tells us that the antioxidants found in açaí enter the human circulation following consumption.

Another study looked at the effects of consuming açaí pulp (100 grams) as a smoothie twice per day for one month in overweight subjects who were at risk for developing metabolic syndrome. Consumption of açaí reduced total cholesterol levels, LDL-cholesterol levels and fasting glucose and insulin levels, however, consumption of açaí had no effect on body weight, blood pressure or levels of C-reactive protein, which is a marker of inflammation (16).

An analysis of cardiovascular parameters in healthy human volunteers following açaí consumption found no impact on blood pressure, heart rate or electrocardiogram endpoints. However, they did find that açaí decreased the standing systolic blood pressure compared to a placebo (17).

I came across a study that was of interest to me as an endurance athlete. This study looked at the effects of supplementation with açaí juice on the blood antioxidant defence capacity in junior hurdlers. Why did these sports scientists investigate this? Well, it is accepted that strenuous exercise is associated with increased production of free radicals and reactive oxygen and nitrogen species (ROS/RNS). Antioxidant supplementation in athletes may prevent exercise-induced tissue injury and assist recovery. These ROS/RNS are also important in muscle adaptation to exercise. So too much ROS/RNS can cause damage but at the same time they are required to signal to our muscles causing adaptation.

In the study I mentioned above elite junior hurdlers drank 100ml of an açaí juice blend daily for 6 weeks. The açaí juice had no effect on performance as assessed by 300m running times, however, it did cause increases in the antioxidant capacity of the plasma of the hurdlers. It also improved the lipid profile by reducing total cholesterol, LDL cholesterol and triglycerides. These young hurdlers were within normal ranges at the start of the study anyway, but these values improved over the 6 weeks. Supplementation with the açaí juice also lowered the levels of the enzymes creatine kinase and lactate dehydrogenase post-exercise. These enzymes are markers of muscle damage. This means that supplementation with açaí may help recovery after training.

Traditionally in the Amazon river basin açaí is used for its antidiarrheal activity. This has not been substantiated in any scientific studies.

To summarize, the human studies conducted on açaí consumption show us that the antioxidants from açaí do enter the blood stream and could potentially have a beneficial impact. These studies also show that açaí may have a cholesterol lowering effect but does not seem to impact cardiovascular outcomes, such as blood pressure or heart rate. Also, açaí may be useful for recovery after exercise and training.

Are there any negative effects from consuming açaí?

Açaí pulp is rich in the essential minerals calcium, iron, magnesium and zinc, while the levels of copper and manganese are exceptionally high. In some parts of Brazil, up to 300mls of açaí pulp can be consumed per day. This means that the daily intake of manganese could be six times the recommended amount. This could be a problem, especially for children, vegetarians/vegans and people with anemia, as iron absorption is impaired by manganese (18).


Açaí certainly is abundant in antioxidants and these compounds are bioavailable in humans. There is also evidence that the juice and pulp from this fruit can lower LDL-cholesterol levels. It is also very nutritious being rich in potassium, magnesium, calcium, phosphorus, sodium and vitamins E and B1, as well as containing unsaturated fatty acids and proteins.

OK, I feel better about spending $12.50 on an açaí bowl, and I like the findings about exercise recovery. Am I going to go out and buy açaí powder/frozen pulp? Maybe – but I would probably save it for directly after training for maximum benefits due to the cost. But remember, other vegetables and berries also contain antioxidants and various vitamins and minerals. And the benefits of regular exercise with bursts of high-intensity are key to optimal health. So don’t feel bad if you are not willing to fork out $50 for açaí powder. You can still be a healthy person in my opinion.

  1. Muñiz-Miret N, Vamos R, Hiraoka M, Montagnini F, & Mendelsohn RO (1996) The economic value of managing the açaí palm (Euterpe oleracea Mart.) in the floodplains of the Amazon estuary, Pará, Brazil. Forest Ecology and Management 87(1-3):163-173.
  2. Del Pozo-Insfran D, Brenes CH, & Talcott ST (2004) Phytochemical composition and pigment stability of Acai (Euterpe oleracea Mart.). Journal of agricultural and food chemistry 52(6):1539-1545.
  3. Schauss AG, et al. (2006) Phytochemical and nutrient composition of the freeze-dried amazonian palm berry, Euterpe oleraceae mart. (acai). Journal of agricultural and food chemistry 54(22):8598-8603.
  4. Schauss AG, et al. (2006) Antioxidant capacity and other bioactivities of the freeze-dried Amazonian palm berry, Euterpe oleraceae mart. (acai). Journal of agricultural and food chemistry 54(22):8604-8610.
  5. Chin YW, Chai HB, Keller WJ, & Kinghorn AD (2008) Lignans and other constituents of the fruits of Euterpe oleracea (Acai) with antioxidant and cytoprotective activities. Journal of agricultural and food chemistry 56(17):7759-7764.
  6. Hu J, et al. (2014) Antioxidant neolignan and phenolic glucosides from the fruit of Euterpe oleracea. Fitoterapia 99:178-183.
  7. de Souza MO, et al. (2012) The hypocholesterolemic activity of acai (Euterpe oleracea Mart.) is mediated by the enhanced expression of the ATP-binding cassette, subfamily G transporters 5 and 8 and low-density lipoprotein receptor genes in the rat. Nutrition research 32(12):976-984.
  8. Feio CA, et al. (2012) Euterpe oleracea (acai) modifies sterol metabolism and attenuates experimentally-induced atherosclerosis. Journal of atherosclerosis and thrombosis 19(3):237-245.
  9. de Oliveira PR, et al. (2010) Effects of an extract obtained from fruits of Euterpe oleracea Mart. in the components of metabolic syndrome induced in C57BL/6J mice fed a high-fat diet. Journal of cardiovascular pharmacology 56(6):619-626.
  10. Fragoso MF, Romualdo GR, Ribeiro DA, & Barbisan LF (2013) Acai (Euterpe oleracea Mart.) feeding attenuates dimethylhydrazine-induced rat colon carcinogenesis. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 58:68-76.
  11. Jensen GS, et al. (2008) In vitro and in vivo antioxidant and anti-inflammatory capacities of an antioxidant-rich fruit and berry juice blend. Results of a pilot and randomized, double-blinded, placebo-controlled, crossover study. Journal of agricultural and food chemistry 56(18):8326-8333.
  12. Poulose SM, et al. (2012) Anthocyanin-rich acai (Euterpe oleracea Mart.) fruit pulp fractions attenuate inflammatory stress signaling in mouse brain BV-2 microglial cells. Journal of agricultural and food chemistry 60(4):1084-1093.
  13. Xie C, et al. (2012) The acai flavonoid velutin is a potent anti-inflammatory agent: blockade of LPS-mediated TNF-alpha and IL-6 production through inhibiting NF-kappaB activation and MAPK pathway. The Journal of nutritional biochemistry 23(9):1184-1191.
  14. Matheus ME, et al. (2006) Inhibitory effects of Euterpe oleracea Mart. on nitric oxide production and iNOS expression. Journal of ethnopharmacology 107(2):291-296.
  15. Mertens-Talcott SU, et al. (2008) Pharmacokinetics of anthocyanins and antioxidant effects after the consumption of anthocyanin-rich acai juice and pulp (Euterpe oleracea Mart.) in human healthy volunteers. Journal of agricultural and food chemistry 56(17):7796-7802.
  16. Udani JK, Singh BB, Singh VJ, & Barrett ML (2011) Effects of Acai (Euterpe oleracea Mart.) berry preparation on metabolic parameters in a healthy overweight population: a pilot study. Nutrition journal 10:45.
  17. Gale AM, Kaur R, & Baker WL (2014) Hemodynamic and electrocardiographic effects of acai berry in healthy volunteers: a randomized controlled trial. International journal of cardiology 174(2):421-423.
  18. da Silva Santos V, de Almeida Teixeira GH, & Barbosa F, Jr. (2014) Acai (Euterpe oleracea Mart.): a tropical fruit with high levels of essential minerals-especially manganese-and its contribution as a source of natural mineral supplementation. Journal of toxicology and environmental health. Part A 77(1-3):80-89.


Strawberry and coconut ‘ice cream’ with low carb coconut cookie dough chunks

Strawberry and coconut ice creamThis dessert is soooo good, yet healthy too. What makes this dessert healthy? Well, my friends, this ‘ice cream’ is made with only frozen strawberries, coconut milk, shredded coconut and is sweetened with the low-calorie sugar alcohol erythritol (read all about why this is my sweetener of choice in my recent post “Which sweeteners are the healthiest to use?”).

This ingredient list means that my version of ice cream contains no refined carbohydrates, contains dietary fibre and has medium-chain fatty acids, which, according to the scientific literature, are metabolized more rapidly than long-chain fatty acids.

But the best part about this dessert is the chunks of delicious low carb coconut cookie dough. Again this cookie dough contains no refined carbohydrates and is high in dietary fibre.

Dietary fibre is important as it helps to feed the beneficial bacteria in your gastrointestinal tract. A recent study conducted by the husband and wife research team from the Department of Microbiology and Immunology at Stanford University, Erica and Justin Sonnenburg, showed that a diet low in dietary fibre, or Microbiota-accessible carbohydrates (MACs), decreases the diversity of the gut microbiota in mice. Reintroducing MACs in to the diet can reverse this loss in diversity. However, after multiple generations, this loss in diversity could not be recovered by diet alone (1). So what does this mean? The Sonnenburgs speculate that generations of a highly processed, highly refined, low-fibre modern diet are contributing to the loss of diversity in the human gut microbiota and may be responsible for the increase in many preventable health problems that are common in today’s society. You can attempt to stop this by eating more whole foods, which retain their fibre component.

You will have to freeze the strawberries, coconut and cookie dough a few hours in advance, so be prepared if you want to make this dessert. I believe it is worth the preparation. Your taste buds and your gut bacteria will be happy!

Strawberry and coconut ‘ice cream’ with low carb coconut cookie dough chunks

Makes 2 small serves


Strawberry and coconut ‘ice cream’

1 cup of strawberries, washed, tops removed and frozen

1 cup coconut milk, frozen in ice cube trays

Extra ½ cup coconut milk

½ tablespoon of erythritol (I use Natvia which is a blend of erythritol with a small percentage of stevia)

½ teaspoon coconut essence

3 tablespoons shredded coconut

Low carb coconut cookie dough

1 cup desiccated coconut

3 tablespoons coconut milk

2 tablespoons coconut flour

½ teaspoon coconut essence

½ tablespoon erythritol


Ice cube trays

Sharp knife

Chopping board

Measuring cups and spoons

Food processor

Cling wrap


  • Freeze the strawberries and coconut milk for at least two hours.
  • Add the frozen strawberries, frozen coconut milk, extra coconut milk, coconut essence and erythritol to the food processor.
  • Process until the ‘ice cream’ is smooth and has a fairly even consistency.
  • Add in the shredded coconut and process briefly to mix through. Divide the ice cream between two bowls and freeze for 30 – 60 minutes before serving (don’t let it get too hard).
  • For the cookie dough, add all the ingredients to the food processor and process until a firm ball forms.
  • Lay a sheet of cling wrap onto a chopping board.
  • Remove the ball of cookie dough from the food processor and place it onto the cling wrap.
  • Roll the cookie dough into a long, thick log with your hands.
  • Wrap the cookie dough in cling wrap and freeze for at least one hour.
  • Chop the cookie dough into chunks and place on top of the Strawberry and coconut ‘ice cream’
  1. Sonnenburg ED, et al. (2016) Diet-induced extinctions in the gut microbiota compound over generations. Nature 529(7585):212-215

Which sweeteners are the healthiest to use?

If you have any interest in your health you should be aware that too much sugar is not good for you. The consumption of excess refined sugars has been shown to cause weight gain, dyslipidemia (elevation of cholesterol, triglycerides, or both, in the blood), glucose intolerance and insulin resistance (1, 2). Unfortunately, we humans have evolved to enjoy sweet tasting things and unless you have amazingly strong will power, there are going to be times that you will want to satisfy your sweet tooth. So which sweetener should you choose and which low calorie sweeteners are the healthiest? Mainstream media has vilified many ‘artificial sweeteners’ so here is a review of the most common sweeteners that are available based on factual, peer-reviewed science.

Nutritive sweeteners (sugars and sugar alcohols)

Sweeteners can be grouped as nutritive and nonnutritive. Nutritive sweeteners contain carbohydrates and therefore calories, while nonnutritive sweeteners (NNS) provide very little to no calories. Nutritive sweeteners are often referred to as sugars, caloric sweeteners and added sugars and include:

  • Glucose – the primary energy source used by our bodies (monosaccharide)
  • Fructose – found in fruit, honey and some vegetables
  • Galactose – found in diary products and some plants
  • Sucrose – occurs naturally in fruits and vegetables and is a combination of glucose and fructose (known as a disaccharide), typical table sugar
  • Maltose – made up of two glucose molecules and is found in molasses
  • Corn based sweeteners – refers to products made from corn, an example is high-fructose corn syrup which is a combination of glucose and fructose
  • Honey – can contain up to 200 substances and is mainly made up of sugars (mostly fructose), water, proteins and amino acids (0.1% – 3.3%) with proline being the most abundant amino acid, organic acids (0.57%), small amounts of vitamins, especially the vitamin B complex (the vitamin content may be reduced due to commercial filtering), minerals (0.04% – 0.2%) including potassium, magnesium, calcium, iron and zinc and phenolic compounds, which act as antioxidants. These compounds can change due to processing and storage of honey. The composition, colour, aroma and flavour of honey depends on the flowers, location and climate, and honeybee species involved in the production (3).
  • Agave nectar – liquid sweetener derived from the sap of either the Agave tequilana or Agave slamina plant containing xylose, fructose, glucose and sucrose (4, 5)
  • Maple syrup – obtained by concentrating the sap collected from certain species of maple trees, contains mostly sucrose, also contains minerals, oligosaccharides, amino acids and phenolic compounds (6)

Sugar alcohols, or polyols, are another form of nutritive sweetener. The energy provided by polyols can vary due to differences in digestibility, metabolism and because polyols are slowly or incompletely absorbed.

Many sugar alcohols exist in nature, but are typically manufactured from sugars to be used as food ingredients. They can be produced chemically (this is not a bad thing just because of the word ‘chemical’ – essentially everything is made of chemicals) or through fermentation by certain species of yeast and bacteria.

Sugar alcohols are incompletely metabolized in humans, meaning they are not completely by broken down to provide energy. For example, 10 – 20% of ingested sorbitol and xylitol and 30 – 40% of ingested mannitol is excreted in the urine (7).

Examples of polyols include:

  • Erythritol (discussed in detail later)
  • Xylitol
  • Mannitol
  • Sorbitol

Following ingestion, polyols are absorbed in varying amounts by the human small intestine. Polyols that are not absorbed from the small intestine reach the colon. In the colon, polyols are fermented by gut bacteria to produce short-chain fatty acids and gases, such as hydrogen and methane (8, 9). Short-chain fatty acids are absorbed and provide energy to the body, so this is why polyols that are not absorbed can still provide calories.

The gases produced from the fermentation of polyols can result in gastrointestinal (GI) symptoms, such as flatulence, cramping, bloating and diarrhea. GI symptoms are likely to occur when more than 10 – 20 grams of polyols are consumed at once. This could be from 1 no-added sugar chocolate bar or 2 no-added-sugar cookies.

Polyols may cause problems for people with Irritable Bowel Syndrome (IBS). Studies have shown that low-FODMAP diets can improve the symptoms of IBS. FODMAPs are fermentable oligo-, di- and monosaccharides and polyols. It is thought that the increase in osmotic load in the colon, meaning an increase in un-absorbable, water-soluble solutes in the bowel that cause an influx of water, and the gas generated during fermentation of polyols could contribute to the symptoms of IBS (10).

Most polyols do not raise blood glucose or insulin levels after consumption, which is why they are a suitable choice for people with diabetes. Mannitol, however, which is broken down into sorbitol and glucose after absorption, can cause a small increase in glucose and insulin levels (11).

Polyols cannot be used as an energy source for bacteria that cause tooth decay, also known as dental caries. Dental caries are the destruction of dental hard tissue by acidic material produced by the fermentation of carbohydrates from the diet by oral bacteria.

Xylitol may actually stop the growth of decay-causing bacteria (12). The evidence shows that chewing sugar-free gum sweetened with polyols immediately after meals can prevent tooth decay because of the production of saliva from the chewing action and because oral bacteria cannot metabolise the polyols into acids (13). This, of course, must be combined with tooth brushing to be effective. It should be noted that there is only a small amount of sugar alcohols present in chewing gum.

Nonnutritive sweeteners (NNS)

NNS provide little energy and have been used since the late 1800’s when saccharine was discovered (14). Prior to the 1970’s NNS were used to sweeten medicines and as a sugar substitute in foods for diabetic patients. Since then, a huge industry has developed for NNS to provide sweetness to food without the calories (15).

NNS can be referred to as artificial, alternative, synthetic, low calorie, non-caloric, sugar-substitute, hyper-intense, high-intensity and high-potency sweeteners. NNS are referred to as high-intensity sweeteners because they are many times ‘sweeter’ than sugar. This term high-intensity sweeteners can be misleading and implies that NNS are some sort of ‘super-normal’ stimuli that over stimulate sweet receptors. NNS are actually high-potency sweeteners, meaning that it takes a very small amount of these compounds to activate the sensation of sweetness. Therefore, NNS are able to provide sweetness without contributing a lot of calories to the diet. NNS are ‘sweeter’ than sugar on a weight-to-weight comparison (16).

Examples include:

  • Aspartame
  • Stevia (steviol glycosides – rebaudioside A and stevioside)
  • Sucralose
  • Acesulfame K
  • Neotame
  • Saccharin
  • Luo han guo extract


My research revealed that aspartame is quite a controversial item. It was approved by the US Food and Drug Administration (FDA) in 1981 for use in a small number of food products. In 1983 it was approved for use in soft drinks, then in all foods in 1996. It is the most commonly used artificial sweetener in the world found in soft drinks, desserts, yoghurts, chewable multi-vitamins, breakfast cereals and tabletop sweeteners. G. D Searle & Company discovered aspartame in the 1970s and conducted 3 studies on rats looking at the potential of aspartame to cause cancer prior to its approval by the FDA (17). The results from these studies were not published in peer-reviewed scientific literature and did not meet the current standards for conducting these types of studies, referred to as carcinogenic bioassays (18). The final reports from these studies were finally made available at the end of 2011 on the website of the European Food Safety Authority (EFSA).

The results from the studies conducted in the 1970s are somewhat dubious. One of the studies showed that female rats feed aspartame daily from 4 to 104 weeks consumed less food, weighed less and had higher death rates than control rats and had an increased incidence of mammary cancers. The other two studies showed no increase in tumors in rats feed aspartame which survived to the end of the study, but again death rates were higher among the rats feed aspartame.

Studies conducted in 1981 showed no increase in the incidence of brain tumors for rats feed aspartame daily for 104 weeks (19, 20).

In 2006 the Cesare Maltoni Cancer Research Center of the Ramazzini Institute (RI) conducted studies feeding male and female rats aspartame for their entire life span starting from 8 weeks of age. Results from these studies showed increased incidences of lymphomas/leukemias and tumors of the renal pelvis in male and female rats and of peripheral nerves in males (18, 21). These results were repeated in 2007 (22). In 2010, the same research center conducted studies on mice and showed that aspartame increases cancers of the liver and lung in males (23). These studies have been criticized by experts in the area, including the FDA and the European Food Safety Authority (EFSA), for a number of reasons such as: the large number of animals used in the studies meant that animals from treatment and control groups were housed under different environmental conditions, there was apparently a high level of infection among the animals used in these studies leading to low survival rates in treated and control groups, specific details of the diets were not provided, there was uncertainty in the diagnosis of some tumor types and a lack of relevance to human cancer risks (24). In defense of the Cesare Maltoni Cancer Research Center of the Ramazzini Institute, they were first to demonstrate carcinogenicity in animals of vinyl chloride and benzene, which are recognized as human cancer causing agents (15).

A recent review by Professor Marina Marinovich, from the Laboratory of Toxicology at the University of Milan concluded that there is no evidence to support an association between aspartame consumption and leukemia, haematopoietic neoplasms, brain cancers, pancreatic cancer, breast cancer or cancers of the digestive tract, endometrium, ovary, prostate and kidneys in humans (25).

Another area of concern regarding aspartame is one of its breakdown products, methanol. However, Professor Marina Marinovich states that a glass of tomato juice provides about 6 times as much methanol as an equivalent amount of diet beverage sweetened with aspartame (25).

So should you be worried about consuming aspartame? I find the animal studies from the Cesare Maltoni Cancer Research Center of the Ramazzini Institute somewhat concerning. However, in the USA the estimated intake of aspartame is 1/10 of the Acceptable Daily Intake (ADI) (26). To reach the ADI an adult would have to drink 12 cans of soft drink per day for their whole life (25). Also bear in mind that the mass media loves a good fear-mongering story and often misinterpret or over interpret scientific publications. The issue, I believe, is that food and drinks containing aspartame, such as diet soft drinks and processed sugar-free desserts, really have little nutritional value. If you use small amounts of aspartame now and then as a low calorie sweetener then the risk to your health is most likely negligible.


The sweet tasting components of stevia are actually the steviol glycosides (rebaudioside A and stevoside) extracted from the leaves of the plant Stevia rebaudiana (Bertoni). The steviol glycosides are not digested or absorbed in the upper gastrointestinal tract meaning these compounds enter the colon intact. The steviol glycosides are then degraded by microbes in the colon to the compound steviol, some of which is excreted in the fecaes while the remainder is absorbed into the circulation. Steviol is then converted to steviol glucuronide, where it is excreted in the urine (27, 28)

The safety of steviol glycosides for use in foods has been extensively evaluated by national and international food safety agencies including the Joint Expert Committee on Food Additives (JECFA), a scientific advisory body of Food and Agriculture Organisation (FAO) of the United Nations, and the World Health Organisation (WHO) (29), as well as in the scientific literature.

As far as I can tell there is no evidence for any potential negative health impacts from consuming the steviol glycosides in the scientific literature for animals or humans. The only study I came across was a recent publication in the journal Molecular and Cellular Endocrinology looking at the effects of the steviol glycosides and the metabolite of these glycosides, steviol, on hormone production by human mammary gland cells and human sperm cells (30). This study was undertaken because the steviol glycosides and steviol have a steroid-like structure. The sex hormones, estradiol and testosterone are examples of steroids. This study found that steviol had an impact on progesterone production in these human cells, however, the cells in these studies were literally bathed in this compound.

Are the results of these studies concerning? In my opinion, probably not, as studies conducted on laboratory animals have failed to show any effect on fertility or reproductive organs. However, as there are studies on the long-term use of stevia in humans, it advisable not to use stevia in excessive quantities on a regular basis. I myself have used liquid steviol glycosides and use an erythritol/steviol glycoside blend as a sweetener in dessert recipes. I also use a plant-based protein powder that is sweetened with steviol glycosides. It is not technically a whole food so I try to use only small amounts (which is easy to do as it is far sweeter than sucrose) and I try not to consume it every day.


Sucralose is a modified version of sucrose. The majority of sucralose (approximately 85%) is not absorbed after it is ingested, and is passed through the body unchanged in the feces (31).

Sucralose is found in the low-calorie sweetener SPLENDA®. Actually, granulated SPLENDA® contains only 1% sucralose and 99% maltodextrin, a starch based carbohydrate. Sucralose is 385 – 650 times sweeter than sugar. Studies have identified a number of potential health issues with sucralose. These issues are:

  • Sucralose may affect the absorption of glucose in laboratory animals, This has not been proven in humans.
  • High-intensity sweeteners, such as sucralose, may disrupt the brains association between sweet-tasting foods and calories. It is proposed that this disruption can lead to weight gain.
  • A study using male rats showed that SPLENDA® can increase the levels of a protein that acts as a pump to remove harmful chemicals from the body, known as P-glycoprotein, and of an enzyme, intestinal cytochrome P-450, responsible for the metabolism of drugs and foreign chemicals. This could cause problems if medications are taken with sucralose as these medications may be metabolized more rapidly and unable to have their intended affect (32).
  • This same study found that SPLENDA® decreased and changed the gut microbiota of male rats after 12 weeks. Bacterial species considered to be beneficial were impacted the greatest (32). The effect of sucralose on the bacteria in the human gastrointestinal tract has not been looked at.
  • The long-term effects of regular sucralose consumption in humans are unknown and build up of sucralose and/or its breakdown products in the body may occur.
  • Sucralose may break down into potentially harmful compounds when heated and the presence of other ingredients can impact on this break down (33).

Due to the number of potential negative health issues associated with sucralose, it is probably best to avoid using this sweetener on a regular basis.

Acesulfame K is a combination of an organic acid and potassium (for the chemists) and was approved for use by the US FDA in 1988 as a tabletop sweetener. In 1998 it was approved for use in beverages and in 2003 it was approved as a general use sweetener (34). 95% of this NNS is excreted in the urine unchanged so it does not provide energy and does not have an effect on potassium intake (35).

Neotame was approved by the FDA as a sweetener in 2002. It is partially absorbed in the small intestine and rapidly broken down in the body and excreted in urine and feces (36).


Saccharin appears to be another controversial NNS. It was the first chemical sugar substitute to be approved and its use was increased during World War I and II because of its low production costs and because sugar was less available. More than 50 studies have been published about saccharin and laboratory rats. From these studies it was shown that high doses of saccharin cause bladder cancer in rats, especially males, when both the parent and the offspring are feed saccharin (37). The National Institute for Environmental Health Sciences found that the mechanism by which saccharin causes cancer in rats is not applicable to humans because rats have a different urine composition and react differently to certain compounds (38). Epidemiological studies in humans have failed to find a direct association between saccharin and cancer risk (38, 39).

Luo Han Guo

Luo Han Guo is a concentrate from the Chinese monk fruit, also known as Siraitia grosvenori, or Swingle fruit extract. It has been recently approved as a sweetener by the FDA and is considered generally recognized as safe (GRAS) (40). A powdered concentrate of Luo Han Guo called PureLo is sold as a sweetener or food ingredient and is estimated to be up to 200 times sweeter than sugar. The sweetness of Luo Han Guo is due to the mogrosides, which are members of the family of triterpene glycosides (41). Interestingly, Luo Han Guo has been shown to have antidiabetic properties in rats by suppressing rises in blood glucose levels (42, 43).

How does a sweetener become approved for use?

Now that I have given you some information of the nutritive and nonnutritive sweeteners that are available, let me tell you about the process involved to bring these products to the market. In order for a food additive, such as sweetener, to be approved, the manufacturer or company must compile and present all the safety data for the proposed use of the additive to the Food and Drug Administration in the US or other regulatory agencies. The FDA requires extensive toxicology studies to be carried out. Toxicology studies look at the absorption, tissue distribution, metabolism and the excretion of the sweetener in the short-term and long-term in animals. If potential issues with a food additive, such as allergic reactions or interactions with medications, are identified, the FDA may require clinical studies in humans to be performed (44).

Three safety aspects are crucial to the FDA approving a food additive: 1. The highest no effect level, meaning the FDA must be able to figure out the highest level of intake at which no adverse effects occur; 2. The Acceptable Daily Intake (ADI), meaning the amount considered safe to consume every day over the course of a lifetime without adverse effects (this amount is determined by the No Observed Adverse Effect Level then multiplying it by 100 so that the ADI is 100 times less than the amount found to have no harmful effects); and 3. The estimated daily intake, meaning the amount of the additive to be added to foods, assuming 100% replacement of sugars and other NNS and the typical consumption of those foods by people of different ages and health status (45).

An FDA ruling may be challenged after approval if new evidence becomes available. The FDA will examine the post-market evidence with the same strictness that pre-market studies received and will consider new data in the context of the entire body of evidence to ensure appropriate risk analysis to protect the health of the public (46).

In Australia, Food Standards Australia and New Zealand (FSANZ) carry out very similar safety assessments before a food additive, such as a sweetener, can be used by consumers (47).

Is erythritol safe?

My sweetener of choice is a blend of the sugar alcohol erythritol with a small percentage of stevia (I typically use Natvia brand). So is erythritol safe to consume?

Firstly, what is erythritol and how is erythritol made? Erythritol is a 4-carbon sugar alcohol and is found naturally in several foods including wine, sake, beer, watermelon, pear, grapes and soy sauce. It is also present in our tissues and body fluids. Erythritol is produced from breaking down corn or wheat starch into glucose which is fermented by safe, food-grade yeast (48).

After ingestion, the majority of erythritol (about 90%) is absorbed from the small intestines. It is not metabolised by our body’s cells, therefore all absorbed erythritol is excreted unchanged in the urine, with only small amounts excreted in the feces. Any unabsorbed erythritol is transported to the large intestine.

Erythritol results in less gas production than other polyols. This is because it seems that erythritol is resistant to fermentation by bacteria found in the human colon (49). This lack of fermentation of erythritol means that it is not converted to short-chain fatty acids and provides virtually no calories.

Erythritol does not raise blood glucose levels or insulin levels in healthy or diabetic individuals (50).

Extensive short-term (28 days) and long-term (up to 2 years) studies on the potential toxicology of erythritol have been conducted in laboratory animals and on human subjects. The results from these studies show that erythritol shows no signs of toxicity, has no effects on reproductive performance or fertility, is well tolerated, and has no cancer-causing potential (48).

The safety of erythritol for use in foods and beverages was confirmed by the Joint WHO/FAO Expert Committee on Food Additives in 1999 (51), the EU Scientific Committee on Food in 2003 (52) and by many other Regulatory Authorities around the world. In the EU, erythritol is authorised for the same uses as other polyols (53).

There is some evidence that consumption of erythritol may reduce dental caries. One study showed that three-year consumption of erythritol-containing candies by 7- to 8-year old children was associated with reduced plaque growth, lower levels of plaque acetic acid and propionic acid, and reduced oral counts of mutans streptococci compared with the consumption of xylitol or sorbitol candies (54). I did notice, however, that this study was funded by the company that made the candies, and I felt that this study was lacking appropriate controls.

The only adverse events that I was able to find related to the consumption of erythritol are diarrhea in adults and children following single high doses; 42 grams for adults and 25 grams in solution for children. This is due to the high osmotic activity of unabsorbed erythritol in the gut, which draws in fluid (55, 56).

I did find one other study that suggested long-term consumption of fructose, acesulfame K, rebaudioside, and erythritol in mice might aggravate the cerebral ischemic injury (stroke). This may partly result from the impairment of endothelial progenitor cells (EPCs) and the reduction of angiogenesis in the ischemic brain (57), meaning that there may be impairment in the development of new blood vessels to the brain.

Conclusions – which sweetener should you use?

Like anything in life, too much of one thing is not good for you. This is especially true for refined sugars and carbohydrates. The occasional ice cream or piece of chocolate cake is not going to be too harmful to your health, but it is advisable to avoid refined carbohydrates as much as possible and focus on nutrient dense food. If you are going to use a sweetener in a recipe then which should you choose?

Out of the nutritive sweeteners, raw honey seems to be the best option. It contains a number of nutritional components, such as amino acids, vitamins and minerals. Maple syrup also has nutritional properties. However, both of these sweeteners provide calories in the form of carbohydrates.

If you are trying to avoid the calories and prefer to use a nonnutritive or low calorie sweetener, then I would go for the sugar alcohol erythritol. Many of the other nonnutritive sweeteners seem to have potential side effects and it is probably best to try to avoid them as much as possible.

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FreeImages.com/Maria Kaloudi

All of your questions about nuts answered

nuts-300x300Nuts and nut butters are featured in many ‘healthy dessert’ recipes online and are often referred to as a health food. On the other hand, reports of nut allergies have increased greatly in the last 10 years, especially among children.

So are nuts really as healthy as they are made out to be and how many should you consume on a daily basis?

I conducted my own research, using only peer-reviewed science published in quality journals, and put together this article, which takes a detailed look at what nuts are composed of and the potential positive and negative health effects from consuming nuts.

What are nuts?

Let’s start with defining exactly what nuts are. Tree nuts are dry, hard fruits with one seed. The most common tree nuts include:

  • Almonds
  • Walnuts
  • Cashews
  • Pecans
  • Pistachios
  • Macadamias
  • Brazil nuts
  • Pine nuts

Peanuts are actually legumes as they grow in the ground, but they have a similar nutrient profile to tree nuts.

Chestnuts are unlike other tree nuts as they are starchy and contain little fat.

What are nuts made up of?

Nuts are a very energy dense food as they contain a high amount of fat ranging from 46% in cashews and pistachios to 76% in macadamia nuts (1).

This fat is predominantly in the form of monounsaturated fatty acids (MUFAs). Hazelnuts, for example, contain 61% total fat content with approximately 90% of those fats being the MUFA oleic acid (2, 3).

Nuts also contain the omega-6 polyunsaturated fatty acid (PUFA) linoleic acid and the short chain omega-3 PUFA α-linolenic acid (ALA). Walnuts are in fact the whole food with the highest content of ALA of all edible plants (1).

As well as being a rich source of unsaturated fatty acids, nuts are a good source of protein, with a high content of the amino acid L-arginine.

Nuts are a rich source of a variety of vitamins and minerals, including tocopherols (a form of vitamin E), folate (a B vitamin), magnesium, zinc and calcium (4). Brazil nuts are an excellent source of the trace element selenium. Daily consumption of just one Brazil nut is sufficient to supply the recommended dietary intake of selenium (5).

Additionally, nuts are abundant in the antioxidant compounds polyphenols (6) and in the plant phytochemicals known as phytosterols (7). The majority of the antioxidants in all nuts are located in the skin, known as the pellicle (8). In walnuts, for example, more than 90% of the total antioxidants are lost when the skin is removed (9).

Raw nuts contain between 3 and 13% dietary fibre, with almonds and pistachios having the highest content (10).

Nuts are naturally low in carbohydrates.

Brief summary: Nuts are an energy dense food containing high amounts of monounsaturated and polyunsaturated fatty acids, protein, especially the amino acid L-arginine, a variety of vitamins and minerals, antioxidants and dietary fibre and are low in carbohydrates.

Nut consumption has been associated with cardiovascular health benefits

The first reports of the health outcomes of nuts were in the early 1990s when two important studies were published: the Adventist Health Study, which related frequent nut consumption with a lower risk of coronary heart disease (CHD) (11) and a randomized clinical trial showing that the intake of walnuts reduced serum cholesterol levels (12).

Since then many studies have been conducted on nut consumption and cardiovascular health.

Large studies conducted in the US investigating associations of dietary components with health outcomes reported a beneficial effect of nut consumption on fatal and non-fatal CHD (8, 13-15). The results from these studies suggest a strong association, not a direct causation, between nut consumption and reduced CHD rates.

Random clinical trials have shown that nut consumption has a cholesterol-lowering effect (16). The consumption of 67 grams of nuts per day (2 small servings) was associated with an average reduction in total cholesterol, a reduction in low-density lipoprotein-cholesterol (LDL-C) (the ‘bad’ form of cholesterol) and a reduction in the ratio of LDL to high-density lipoprotein (HDL).

The cholesterol-lowering effects of nuts were shown to be greater for subjects with higher LDL-C levels and for those subjects following a typical ‘Western’ diet rather than a Mediterranean diet. In other words, if you are not obese but have high LDL-C levels and are following a Western diet, consisting of predominantly refined cereals and sugars, refined vegetable oils, fatty meats, dairy products and salt (17), then you will benefit the most from substituting calories from saturated fats with nuts.

A recent review found that there is insufficient evidence to indicate that increased nut consumption will reduce the risk of cardiovascular disease (CVD) in healthy individuals (18).

The mechanisms explaining how nut consumption can improve blood lipid and lipoprotein profile and cardiovascular health are not clear.

In the 1990s it was thought that dietary saturated fatty acids were a main cause of cardiovascular disease (CVD) (19). Therefore, it was recommended that dietary saturated fatty acids be replaced with MUFAs and PUFAs, such as those found in nuts. However, it is now clear that excess carbohydrates, especially when combined with saturated fatty acids, are more detrimental to cardiovascular health (20-24). Therefore, it is hard to say whether the MUFAs and PUFAs in nuts are the cause of improved blood lipid/lipoprotein profiles or if the elimination of certain foods, such as refined carbohydrates and saturated fatty acids, are the cause.

The other beneficial compounds in nuts, such as the polyphenols, may also contribute to cardiovascular health (25-28).

Brief summary: Frequent nut consumption has been associated with reduced rates of coronary heart disease in large epidemiological studies. In individuals with elevated LDL-C levels who are eating a typical Western diet the substitution of saturated fats with nuts may improve blood lipid/lipoprotein profile and improve cardiovascular health.


Nut consumption is not associated with a reduced risk for type 2 diabetes

Several recent major studies have found no association between nut consumption and the risk of type 2 diabetes (29-31).

Will eating nuts cause weight gain?

Although nuts are high in fat and calories, multiple epidemiological studies have shown that frequent nut consumption (greater than 2 servings per week) is not associated with an increased body mass index (BMI) or risk of obesity (32-34).

In clinical studies where small servings of nuts were incorporated into the diet, subjects showed less weight gain than predicted due to the extra energy provided by the nuts (35-39).

These findings may be due to the high amounts of unsaturated fatty acids, dietary fiber and protein found in nuts making them a very satisfying food and preventing hunger, overeating and snacking on less nutritious foods (40).

Also, nuts must be chewed thoroughly before swallowing, and chewing activates mechanical, nutrient and sensory signaling systems that may alter appetite (41).

There is some evidence to suggest that MUFAs and PUFAs are oxidized in the body more rapidly than saturated fatty acids (42), which may also explain why nut consumption is not associated with weight gain.

The cell walls of nuts, which are composed of non-starch polysaccharides (dietary fibre) and enclose the fats, could also explain why nut consumption does not appear to cause weight gain. Additional fat has been found to be excreted in the feces of healthy subjects eating an almond-rich diet (43). Further research into this found that a large portion of the almond cell walls remained intact following chewing and digestion. This prevents the release of the fats from inside the almond cells meaning less fat is absorbed in the gastrointestinal tract (44).

Brief summary: For a number of possible reasons, including the satisfying effects of nuts, the chewing of nuts, the MUFAs and PUFAs in nuts and the cell walls of nuts, the incorporation of a small serving of raw nuts on a daily basis into a healthy diet not exceeding calorie requirements is unlikely to lead to weight gain.

Nut allergies

More than 1% of the US population suffers from peanut and/or tree nut allergy. Peanut and tree nut allergies can result in serious life-threatening reactions (45, 46).

The reports of peanut and tree nut allergy have greatly increased in children in the last 10 years (47). The reasons for this increase are not completely known. An increase in awareness and reporting by parents and an increase in nut consumption may be contributing factors (46).

A number of alternative theories attempting to explain the increase in nut allergies have also been proposed. A decline in the diversity of the gut microbiota (the bacteria found in the gastrointestinal tract) of the infant (48, 49) and/or of the mother during pregnancy, increases in maternal obesity rates (50) and changes in the timing of the introduction of solids to infants have all been suggested to contribute to the increase in nut allergies in recent years (51).

Nut allergy most commonly presents in the first five years of life. More than 90% of children with nut allergy will have a history of eczema, asthma, rhinitis (inflammation of the mucous membrane inside the nose) or another food allergy (52).

If a child is allergic to nuts, they will show a reaction upon their first ingestion of nuts. Typical signs and symptoms of an allergic reaction to nuts include erythema (redness of the skin, usually in patches), hives (pale red, raised itchy bumps on the skin), swelling of the lips, face and around the eyes, itching of the skin and throat, hoarse voice, coughing, sneezing, nausea and diarrhea. These symptoms will develop within minutes of exposure (53).

Peanut and tree nut allergy can be diagnosed by a combination of medical history, physical examination and diagnostic testing, such as the skin prick test (54).

The best timing for the introduction of ‘allergenic foods’ (nuts, eggs, cow’s milk and shellfish) to infants is an area that is currently under intense investigation and is still yet to be determined (55). Although the World Health Organization (WHO) recommends the introduction of solids to infants after the age of 6 months (56), experts in the field of allergy research recommend that infants should be introduced to solids around the age of 4 – 6 months and that ‘allergenic foods’ do not need to be avoided by infants when solids are introduced (57-59).

Avoiding nuts during pregnancy (if the pregnant woman is not allergic) does not appear to decrease the risk of nut allergy in children (55). In fact, pregnant women, who are not allergic to nuts, who consume nuts during the early stages of pregnancy may actually reduce the risk of nut allergy in their children (60).

There is no treatment for nut allergies. The only way to manage peanut and tree nut allergy is by avoiding these foods and being prepared to handle an accidental ingestion.

Research is being conducted into treatments for nut allergies. One treatment method that is currently under investigation is allergen-specific immunotherapy. This involves exposing the allergic individual to small amounts of the substance that they are allergic to, known as an allergen. Studies have shown some success with allergen-specific immunotherapy in people with peanut allergy (61, 62) and hazelnut allergy (63, 64), but further research is needed before this can be considered as a treatment option.

Brief summary: Peanut and tree nut allergies can cause serious life-threatening reactions and reports have increased among children in the last 10 years. Most children with a nut allergy will have a history of eczema, asthma or another food allergy. Avoiding nuts during the first 6 months of an infant’s life or during pregnancy does not seem to reduce the risk of nut allergy in children. There is currently no treatment for nut allergy, but this is an active area of research.

Nuts can be contaminated with harmful aflatoxins

Aflatoxins are toxic substances produced by the fungi Aspergillus flavus, Aspergillus parasiticus and Aspergillus nomius.

These toxins cause dangerous diseases in humans, such as liver cancer. Aflatoxins can also cause disease in animals.

Peanuts and tree nuts are one of the food crops that can be contaminated with aflatoxins.

Contamination with aflatoxins occurs mainly in tropical and subtropical regions of the world. Contamination can occur during harvesting, drying or storage of food crops. Poor agriculture and harvesting practices, as well as improper drying, handling, packaging, storage and transport of food crops can result in contamination with aflatoxins (65, 66).

Once the food has been processed, further contamination with aflatoxins is unlikely as long as the food items are stored correctly (67).

Developing countries located in tropical regions are at the greatest risk for exposure to foods contaminated with aflatoxins (66).

Pistachios are the main source of dietary aflatoxins (68). In 2010, the USA banned the import of all pistachios from Iran where contamination of these nuts is a major problem.

Most countries in the world, including the USA, the European Union and Canada, have strict regulations to control the presence of aflatoxins in food to protect human and animal health (69). However, there are reports of nuts and nut products contaminated with aflatoxins in Sudan (70, 71), Iran (72), Malaysia (73), Tunisia (74), Pakistan (75) Qatar (76) and South Korea (77).

More sensitive and rapid methods for the detection of aflatoxins in food products, including nuts, are currently being developed (78).

Brief summary: Peanuts and tree nuts can be contaminated with harmful aflatoxins, which are produced by fungi. Contamination of nuts with aflatoxins mainly occurs in subtropical and tropical developing countries that have poor agriculture and harvesting practices. Most countries in the world have strict regulations to control the presence of aflatoxins in food.


Nuts are naturally low in carbohydrates and contain a number of potentially beneficial compounds, including monounsaturated and polyunsaturated fatty acids, polyphenols, phytosterols, an array of vitamins and minerals and dietary fibre. Some of these compounds may explain the association between nut consumption and the reduced risk of cardiovascular disease, however, no direct causation has been clearly identified.

Reports of peanut and tree nut allergies have increased among children in the last 10 years. The exact reasons for this increase are unknown. The research suggests that avoiding nuts during the first 6 months of an infant’s life or during pregnancy does not reduce the risk of nut allergy in children.

Tree nuts and peanuts are one of the foods most commonly contaminated with harmful aflatoxins produced by fungi, which can cause dangerous disease such as liver cancer. Contamination of nuts with aflatoxins is most likely to occur in subtropical and tropical developing countries that have poor agriculture and harvesting practices.

Nuts can be included as a part of a healthy diet, especially low carbohydrate diets. Raw nuts as a snack are a far better option than many other convenient snack foods containing refined carbohydrates and trans fatty acids. Although studies have shown that nuts are not associated with increased body mass index (BMI) or risk of obesity, let’s not forget that nuts are very high in calories and should be limited to 1- 2 servings per day, particularly if you are trying to lose weight.

 So now that you have had all your questions about nuts answered, here is a link to my recipe for a whole food Chicken cashew nut featuring, of course, cashews (but not too many).


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Are exercise, intermittent fasting and intellectual challenges the secrets to lifelong brain health?

healthy brainI read an intriguing article recently published in the journal Ageing Research Review written by the Chief of the Laboratory of Neurosciences at the National Institute on Aging AND Professor at the Department of Neuroscience at the Johns Hopkins University School of Medicine. This amazing person is Dr Mark P. Mattson. The article was entitled “ Lifelong Brain Health is a Lifelong Challenge: From Evolutionary Principles to Empirical Evidence” (1).

This article describes the many lines of evidence indicating that regular exercise, energy restriction and intellectual enrichment sustain brain health and function during aging and may prevent neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases.

Dr Mattson believes that the brain is hardwired to function at a peak state when the individual feels hunger. Our human ancestors and wild animals had to survive by being able to locate and acquire food. Therefore, evolution selected for those members of a species that were able to outsmart and outrun their prey. This is in contrast to modern humans and domesticated animals where food is always easily available.

There is substantial evidence supporting Dr Mattson’s hypothesis from experiments performed with laboratory rats and mice. Typically mice and rats under laboratory conditions do not perform any exercise and eat as much as they like. When given running wheels, rats and mice will run up to 10 – 20 kilometers per day and mice that run show improved spatial learning and memory and increases in synaptic transmission and synapse number (a synapse is the junction between two nerve cells). Running also stimulates the growth of neural stem cells and increases the number of functional brain cells. Daily exercise can also prevent the decline in cognitive function that occurs with age in mice and rats.

Exercise can prevent the onset of disease in experimental models of Alzheimer’s disease, Parkinson’s disease and stroke in laboratory animals.

Dietary energy restriction has been shown to have similar effects on mice and rats, and the combination of exercise and energy restriction has been shown to have a greater impact on brain function than running or energy restriction alone.

Animal studies also suggest that intermittent exercise, fasting and intellectual enrichment can enhance recovery from traumatic brain injuries.

The article describes the mechanisms by which exercise, energy restriction and intellectual enrichment enhance cognitive performance during aging. I won’t go in to the details, but these mechanisms include the release of neurotrophic factors (proteins responsible for the growth and survival of developing neurons), activation of stress responses and signals received from other parts of the body, such as ketones from the liver.

Data from human studies suggest that people who exercise regularly during their adult life have a reduced risk of Alzheimer’s and Parkinson’s disease. To date there has been no studies looking at the impact of intermittent energy restriction on Alzheimer’s and/or Parkinson’s disease, however, there is evidence suggesting that overeating is a risk factor for both of these neurodegenerative disorders. Furthermore, intellectually challenging occupations and social engagement may also help prevent Alzheimer’s disease in later life.

Dr Mattson concludes with several points about the difficulties associated with conducting well-designed human trials involving vigorous daily exercise and intermittent fasting, which I agree with. These include the current eating patterns of three meals a day with snacks that we are all so accustomed to, the lack of physical activity required in most occupations, the over consumption of processed foods, which is heavily promoted and marketed by the food industry and the focus on disease treatment rather than prevention.

So what does this all mean to you? How can you use this information to prolong the life of your most valuable asset – your brain? Take Dr Mattson’s advice and ensure you are engaging in regular exercise, especially exercise that is mentally challenging and vigorous. For example, don’t just go for a long, slow walk. Instead choose a route with hills and sprint up the hills then recover on the way down.

What about intermittent fasting? Fasting may sound daunting to some people but I have incorporated this into my life by skipping lunch during the week. While I am busy and occupied at work I do not feel the need to eat lunch and have learnt to suppress my feelings of hunger. This becomes easier the more you do it and I am now completely comfortable with this experience.

And perhaps watching television in the evenings is not the most intellectually challenging pastime to be engaging in. Why not read a great book instead?

Try incorporating daily exercise, bouts of food deprivation and intellectually stimulating activities into your life to enhance the lifelong health of your brain.


  1. Mattson, M. P. (2015). Lifelong Brain Health is a Lifelong Challenge: From Evolutionary Principles to Empirical Evidence. Ageing Res Rev. 20: 37-45.

Exercise has a beneficial effect on the diversity of the human gut microbiota

Human-gut-bacteriaI have an interest in the human gut microbiome and the influence that the composition of this dynamic ecosystem has on human health and disease. As such, I am always keeping an eye out for interesting studies and articles relating to the gut microbiome and/or microbiota. The following article was particularly intriguing to me as a molecular microbiologist and as an amateur athlete: ‘Exercise and associated dietary extremes impact on gut microbial diversity’ published in 2014 in the journal Gut (1).

The adult gut microbiota contains up to 100 trillion microorganisms, including at least 1000 different species of known bacteria. Humans have coevolved with these microbes for thousands of years and the bacteria in our gut play very important roles in digestion, development of the immune system and protection against some infectious agents. Advances in DNA sequencing technology have greatly expanded our ability to identify the microorganisms in the human gut and to understand the complex interplay between these microbes and our own cells.

Diversity of the gut microbiota has been associated with good health status. On the other hand, a loss of gut microbial diversity has been linked to a range of disease states including Crohn’s disease, ulcerative colitis, irritable bowel syndrome and infection with Clostridium difficile (2-5). Furthermore, obese people have fewer types of microbes in their guts than lean people (6, 7). Reduced diversity of the gut microbiota during infancy has been associated with an increased risk for the development of allergies in children (8).

Although it is known that diet plays a huge role in shaping the gut microbiota, the impact of exercise has received much less attention. The above study is one of only a few that has investigated the impact of exercise on the gut microbiota and is the only study conducted on humans to date. This study looked at the faecal microbiota of a professional rugby team while in a regulated environment of a preseason camp. The microbiota was compared to two control groups: one matched for athlete size with a comparable body mass index (BMI) and another group matched for age and gender. It should be noted that the average BMI of the elite rugby players in this study was 29.1, which is considered overweight and almost in the obese category.

Athletes were found to have greater gut microbiota diversity when compared to the control groups. The elite athletes also had lower inflammatory markers despite elevated levels of plasma creatine kinase, a marker of extreme exercise, and had improved metabolic markers. The athletes had a greater intake of dietary protein which also likely influenced gut microbiota diversity.

The findings from this study are that exercise and diet impact gut microbial diversity. It appears that microbiota diversity is an indicator of health, so if you are considering starting an exercise regime or getting back into sport in the new year then hopefully this study will motivate you. Exercise will not only improve your fitness and cardiovascular health, but it may also enhance the diversity of the microbes in your gut.

  1. Clarke SF, et al. (2014) Exercise and associated dietary extremes impact on gut microbial diversity. Gut 63(12):1913-1920.
  2. Dicksved J, et al. (2008) Molecular analysis of the gut microbiota of identical twins with Crohn’s disease. The ISME journal 2(7):716-727.
  3. Frank DN, et al. (2007) Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proceedings of the National Academy of Sciences of the United States of America 104(34):13780-13785.
  4. Carroll IM, et al. (2011) Molecular analysis of the luminal- and mucosal-associated intestinal microbiota in diarrhea-predominant irritable bowel syndrome. American journal of physiology. Gastrointestinal and liver physiology 301(5):G799-807.
  5. Chang JY, et al. (2008) Decreased diversity of the fecal Microbiome in recurrent Clostridium difficile-associated diarrhea. The Journal of infectious diseases 197(3):435-438.
  6. Ley RE, Turnbaugh PJ, Klein S, & Gordon JI (2006) Microbial ecology: human gut microbes associated with obesity. Nature 444(7122):1022-1023.
  7. Turnbaugh PJ, Backhed F, Fulton L, & Gordon JI (2008) Diet-induced obesity is linked to marked but reversible alterations in the mouse distal gut microbiome. Cell host & microbe 3(4):213-223.
  8. Bisgaard H, et al. (2011) Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age. The Journal of allergy and clinical immunology 128(3):646-652 e641-645.