blood sugar

Why fruit juice won’t give you cancer.

But it can protect you against it.

But it can protect you against it.

You may have noticed the carbohydrate fearing headline stating that - "One small glass of juice a day raises cancer risk, " yesterday. Do you know when you’ve been tangoed?

This is based upon the study by Chazelas et al (Chazelas et al 2019) and being used to justify the swathe of dogmatic headlines in the press.Apart from the study being based on food questionnaires (mean food log was 5.6 days over 5 years hardly conclusive) which are not reliable indicators of actual consumption, the authors suggest that the mechanisms that might drive the association are as follows.

1.    Excessive sugar consumption could contribute to obesity driven mechanisms. There's no doubt that excess carbohydrate, fat and protein contribute to obesity when an EXCESS of calories are consumed (and the other multifactorial issues associated with obesity.

2.    Sugar from juice contributes to increased glycaemic load and inflammation. This point doesn't add up because many fruit juices have a low glycaemic load, associated with anti- inflammatory responses (polyphenols, vitamin c, capacity to lower endotoxins, improve blood sugar regulation and cholesterol levels). Many grains have higher glycaemic loads and index than juices. So is this really a valid argument?

Of the 101, 000 or so participants the increased risk associated with sugary drinks was found in those who exercised less. In an important factor, if you combine over consumption and decreased activity. Another point that the authors suggest on sugary drinks is that additives to sweetened beverages like sodas could also contribute to risk. Indeed a valid point.

It starts with a hint of truth and a headline or meme tends to become written in folklore, the myth of the carbohydrate rich food churning out death in its path. These small, half or even quarter truths often disappear when you scratch beneath the surface. That’s why I actively encourage carbohydrate and specifically carbohydrate consumption in my programs. Even most people I have met rarely chug down large amounts of fruit juices in isolation and even if glycemic index\load were an issue, when you consume carbohydrate rich foods with proteins and fats, these concepts are somewhat irrelevant.

Orange juice (or any juices) is one of those foods that still seems to be getting a bad rap but many people who demean its nature often fail to look at the studies that have shown it to be protective. You might have heard...but the sugar levels or but it’s acidic. Just take a look at the tabloid’s permanent vilification of the simple juice drink, which is based on half-truths of small increased risk with limited data. To play devil’s advocate, there’s no doubting that some people with less money available have been seduced into purchasing more junk food. It’s cheap, it’s filling and it’s full of sugar, vegetable oils, preservatives, GMOs, fillers, emulsifiers, additives like flavouring, enhancers, gums and much more. Yet still, the sugar is the demon in this list. Not even the pollution that’s shown to increase cancer, heart diseases, diabetes and neurodegenerative diseases, it’s still sugar and even if you drink fruit juice, it’s the sugar that will kill you.

So, with that in mind let’s consider what a simple food like orange juice could do to hasten, I’m sorry I meant prevent neurological and metabolic decline. Let’s first add some context. It should be no surprise that if you just drink large amounts of juice on their own, without balancing their ability to enter the blood stream with fats and or proteins, it isn’t going to be as beneficial. This is also why throwing large amounts of sweetened fizzy drinks down one’s neck can be problematic. The Glycemic index becomes redundant when you add another food into the mix, therefore drinking fruit juices with fats and proteins helps to normalise blood sugar responses in isolation. So why orange juice? Here are just a couple of reasons

Orange juice decreases inflammation

Eating a variety of foods has the capacity to increase inflammatory and damaging agents like endotoxin. Endotoxin or lipopolysaccharides is well known to increase in high fat and carbohydrate meals, especially so when fibrous poorly digested foods are consumed. High fat diets also induce endotoxin, and this is well known to induce intestinal hyperpermeability or the more well-known leaky gut syndrome. Consumption of orange juice appears to significantly reduce the levels and effects of inflammation induced by endotoxin (Ghanim et al., 2010) . Unfortunately, many foods are often kept stable longer with additives like carrageenan and gums, which also promote increased endotoxin.

Orange juice attenuates metabolic dysfunction

 “ Despite media concern, daily orange juice consumption did not result in adverse metabolic effects, despite providing additional dietary sugars. Data from epidemiological and in vitro studies suggest that orange juice (OJ) may have a positive impact on lipid metabolism. “ (Simpson, Mendis, & Macdonald, 2016)

During times of stress, under eating or consuming foods low in carbohydrates the response is to liberate energy from stored fats in the form of triglycerides. As metabolism becomes compromised high levels of triglycerides are known to be present in blood sugar dysregulation. There’s much in the press to suggest that sugar from fruit juice consumption increases cardiac risk but there are many studies that suggest otherwise, with the observed effect being reduced triglycerides and cholesterol (Aptekmann & Cesar, 2013). The cardiac protective factors aren’t limited to orange juice alone, pomegranate and other juices also seem to offer similar results (Moazzen & Alizadeh, 2017)

Orange juice decreases carcinogen production

A very relevant and protective mechanism of orange juice (and others) and fruit peel consumption is the decreased risk of gastrointestinal cancers (Xu, Song, & Reed, 1993). Nitrates and nitrates are naturally occurring compounds found in a variety of foods. Nitrates are often used in preservatives and sodium nitrites are ubiquitous in preserved meats and have a significant relationship between cancers in many of the mucosal areas including the mouth, bowel and lungs.. Nitrates have been implicated in not just intestinal and stomach cancers but increasingly thyroid cancers (Hernández- Ramírez et al., 2009). This occurs through increases in N-nitroso compounds (NOC) which increase the capacity of cell mutation but there are extensive studies that show many classes of NOC inhibitors which include vitamin e and vitamin C that negate that risk.

Of course, for optimal effects, ensuring adequate protein and fats are consumed will always be beneficial. We’ve known that compromised blood sugar and insulin responses are rarely to do with consuming carbohydrates. Unless excessive eating and obesity are the association, there’s plenty more relevant relationships such as environmental pollutants and other stressors that show a clear effect on all aspects of metabolism and increased metabolic disease. Yet many people seem intent on shooting the messenger and vilifying protective carbohydrates such as fruit juice.

 

References: 

 1.    Aptekmann, N. P., & Cesar, T. B. (2013). Long-term orange juice consumption is associated with low LDL-cholesterol and apolipoprotein B in normal and moderately hypercholesterolemic subjects. Lipids in Health and Disease. https://doi.org/10.1186/1476-511X-12-119

2.   Chazelas Eloi, Srour Bernard, Desmetz Elisa, KesseGuyot Emmanuelle, Julia Chantal, Deschamps Valérie et al. Sugary drink consumption and risk of cancer: results from NutriNet-Santé prospective cohort BMJ2019; 366 :l2408

3.    Ghanim, H., Sia, C. L., Upadhyay, M., Korzeniewski, K., Viswanathan, P., Abuaysheh, S., … Dandona, P. (2010). Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and toll-like receptor expression. American Journal of Clinical Nutrition. https://doi.org/10.3945/ajcn.2009.28584

4.    Hernández-Ramírez, R. U., Galván-Portillo, M. V., Ward, M. H., Agudo, A., González, C. A., Oñate-Ocaña, L. F., … López-Carrillo, L. (2009). Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City. International Journal of Cancer. https://doi.org/10.1002/ijc.24454

5.    Moazzen, H., & Alizadeh, M. (2017). Effects of Pomegranate Juice on Cardiovascular Risk Factors in Patients with Metabolic Syndrome: a Double-Blinded, Randomized Crossover Controlled Trial. Plant Foods for Human Nutrition. https://doi.org/10.1007/s11130-017-0605-6

6.    Simpson, E. J., Mendis, B., & Macdonald, I. A. (2016). Orange juice consumption and its effect on blood lipid profile and indices of the metabolic syndrome; A randomised, controlled trial in an at-risk population. Food and Function. https://doi.org/10.1039/c6fo00039h

7.    Xu, G. P., Song, P. J., & Reed, P. I. (1993). Effects of fruit juices, processed vegetable juice, orange peel and green tea on endogenous formation of N-nitrosoproline in subjects from a high-risk area for gastric cancer in Moping County, China. European Journal of Cancer Prevention. https://doi.org/10.1097/00008469-199307000-00007

 

 

Chronic stress, appetite suppression, control and metabolic inflexibility.

It was the famous stress scientist Hans Selye who suggested that stress can be a positive or negative force. But how do we know whether we are dealing with stress effectively? There’s a common theme among clients both male and female who have got used to feeling in control of their health by suppressing appetite, symptoms and a false sense of health by perhaps feeling in control. Is this control a false economy? A well-known symptom of stress is a loss of appetite and skipping breakfast, it feels better to perpetuate the production of stress hormones like adrenaline and cortisol to liberate energy from stored fats and stride through the day with their endorphin like qualities. A common theme of females suffering from poly cystic ovary syndrome (PCOS) is chronic irregular eating or over eating in the obese. High stress can be chronic and perceived as the norm. I’ve observed the former in my eldest daughter through under eating as a product of emotional stress

‘For those habituated to high levels of internal stress since early childhood, it is the absence of stress that creates unease, evoking boredom and a sense of meaningless. People may have become addicted to their own stress hormones, adrenaline and cortisol, Hans Selye observed. To such person’s stress feels desirable, while the absence of it feels like something to be avoided.’ Gabor Mate

It should come as no surprise why some studies suggest that short term fasting, and calorific restriction seem to be productive in reversing aspects of inflammation and auto immune disease. When the body is stressed even eating certain foods becomes stressful. Dairy, sugar, fruits, grains all get the blame. I feel better when I don’t eat these some say. I feel better when I don’t eat others say. Is it the food or is it you? Can you be so fragile that eating some fruit for example is enough to send your biology into a tail spin. Eating sugar in excess can be problematic but then so can eating fat or anything in excess.

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A foundation of good health is built upon biological flexibility, potential and far away from equilibrium states.

The inability to utilise carbohydrate is a snapshot of the inflexibility of an individuals’ metabolism and not the carbohydrate. Evolutionary biology has provided efficiency by aerobic metabolism of carbohydrate and fat. The loss of efficient use of carbohydrate/sugar is the hallmark of a loss of function or flexibility and the chronic use of fats as a fuel is problematic due to increased oxidation of these lipids which can damage the aerobic apparatus within the mitochondria. The Randle cycle or glucose fatty acid cycle should allow flexibility between using either fats or carbohydrate as a fuel (Randle, Garland, Hales, & Newsholme, 1963). It’s often the lack of flexibility, decreased oxidation of carbohydrate and perpetual use of fats that damage the energy producing cells. Saturated fats are the preferred fuel of aerobic (oxidative) metabolism but in aggressive metabolism of cancer cells, unsaturated fats are utilised perpetuating the damage, promoting inefficient glycolysis or anaerobic metabolism that creates the acidic state of the cell.

The dogma that persists in nutrition circles is not based on sound reasoning but limited ideas that look at short term studies related to carbohydrate restriction. When a system loses its capacity to regulate sugar, we blame sugar instead of looking at the variety of factors that are responsible for degraded biology, carbohydrate utilisation and insulin responses.

Whether excessive exercise or inadequate nutrition the end result may be similar and its effects are far reaching into metabolism, cardiovascular, sexual and reproductive physiology.

By improving life conditions (in many ways) the hormones of pleasure can have a bigger role in our physiology. I think the experience of pleasure (whatever capacity for pleasure there is) increases the ability to experience pleasure, but I don't offer this with much hope as a therapeutic approach, since I know of people who say that running to exhaustion makes them "feel good" - neither "feeling good" nor "having orgasms" has a clear meaning, at present. Ray Peat

I’m not suggesting that going long periods without eating are necessarily bad, nor if you enjoy running is that bad either. Context is key. If you enjoy running run. If you have the capacity to go long hours without eating, then do that too. However if you have a system that lacks flexibility these actions can be problematic.

Have you ever considered not engaging in intense exercise for a couple of weeks to see how your body really feels?

I think this is a useful test to discover where your biology is really at. It can help determine whether you have been propping up a dysfunctional biology with intense exercise that falsely elevates your body temperature through activation of the sympathetic stress pathway. Slowing down and just focusing on walking and a few stretches shouldn’t feel stressful. Equally an individual who switches to eating regularly every 3 hours or so with the same amount of calories they were previously eating shouldn’t feel stressful. We all have patterns, routines and to the extent that they are effective or not is dictated by the metabolic flexibility that one should have. I’ll also suggest that metabolic flexibility could be analogous to emotional flexibility and mood states. A sign of improvements to metabolic flexibility and flux is return of energy, ability to tolerate exercise, good sleep, libido and emotional responses among other aspects of function. How do you know if it’s working? This diagram suggests what drivers are necessary and how to overcome your unwanted symptoms with the right inputs.

Metabolic inflexibilitY.jpg

Some patience seeking the return of these aspects of function is needed. After all, if you have spent decades constrained by negative symptoms then it may take more than a few weeks or months to fully resolve these patterns. In addition to the foundational work on hormones and chemistry, some people might find a need to address belief systems or require counselling for trauma or emotional grief to help resolve emotional stressors.

 References

Mate, G. (2008). In the realm of hungry ghosts. Close encounters with addiction. Canadian Family Physician.

Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963). The glucose fatty-acid cycle its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. The Lancet, 281(7285), 785–789. https://doi.org/10.1016/S0140-6736(63)91500-9

Peat, R. (1997). From PMS to Menopause: Female Hormones in context.

Selye, H. (1987). Stress without distress. In Society, stress, and disease, Vol. 5: Old age. (pp. 257–262). http://doi.org/10.1080/00228958.1983.10517713

 

Gestational diabetes and metformin-Is that the best that medical thinking has to offer?

Gestational diabetes or elevated blood sugar is often treated with metformin to improve blood sugar levels and considered the standard approach to treating gestational diabetes. The research suggests that it has little negative effects on the pregnant mother. However, does significant risks to both mother and baby if the incidence of premature birth count? Here are a few aspects to consider regarding the use of metformin to control blood sugar during pregnancy. A study of patients receiving a dose of metformin, combination of Clomiphene citrate (CC) and metformin both faired better than CC alone for the induction of ovulation (Neveu, Granger, St-Michel, & Lavoie, 2007).  As the combined group showed no benefit compared to metformin alone, one might consider that metformin alone may be considered for the positive effects.

In another study metformin and diet interventions showed a significant outcome compared to non-metformin-diet interventions. The metformin diet showed a reduction of 14 adverse events in a group of 76 expectant mothers, compared to the non-treated group of 36 adverse events out of 76 pregnancies (Glueck et al., 2013).

Thatcher and Jackson (Thatcher & Jackson, 2006) compared pregnancies of 188 women. 61 experienced miscarriages and 11 of those had stopped taking metformin, suggesting other abnormalities beyond metformin’s actions. 81% of women with pregnancies before metformin, 67% had prior miscarriages. 37% of these also miscarried again. Whilst metformin appeared to show minimal effects to mother and foetus 22% were born prematurely.

Whilst metformin has shown favourable outcomes in PCOS states, questions around pertinent biological mechanisms should warrant further discussion. It’s well known that two key endocrine actions may be compromised during the failure to achieve full gestation. Estrogen induces hypoxia in the uterus (Peat, 1997) and failure to produce adequate progesterone to counter the effects of estrogen may be implicated in the commonly fragile time around weeks 9-10 of pregnancy and incidence of miscarriage.

A concern of metformin are its affect transplacentally. Metformin appears to influence testicular size in males and affects sertoli cells. In females it may also lead to decreased androgen synthesis. Birth weight percentile is also significantly lower in pregnancies treated with metformin (Bertoldo, Faure, Dupont, & Froment, 2014)I Metformin has generally appeared safe in expecting mothers but considerable concern should be made regarding its long term effects to offspring and development most notably to reproductive tissues.

Hypothyroidism is a key factor in maintenance of pregnancy and alongside progesterone, thyroid hormone deficiency can be implicated in poor cellular energetics, production of adenosine triphosphate (ATP) and blood sugar regulation. There remains much debate about the issue of subclinical hypothyroidism, values and when to treat and perhaps metformin’s role despite showing some promises may be treating a symptom related to insulin sensitivity.

So perhaps these questions might be more pertinent before prescribing an agent that shows potentially negative effects to the fetus?

  1. What is the nutrition of the mother, is it enough and does it contain enough nutrients to enhance/maintain adequate progesterone/thyroid production?
  2. Is estrogen increasing at a rate that suppresses progesterone/thyroid levels and persistently decreases insulin sensitivity?
  3. Is there enough carbohydrate in the diet to ensure that carbohydrate is effectively utilised instead of persistent conversion of fats, increasing overall stress to both mother and fetus?
  4. Are the values of hypothyroidism and the identification of subclinical/functional hypothyroid factors appropriate?
  5. Is gestational diabetes a reflection of the above points?

The use of metformin, without questioning these mechanisms, remains at best a reduced treatment that fails to address a range of biological interactions and function.

References:

Bertoldo, M. J., Faure, M., Dupont, J., & Froment, P. (2014). Impact of metformin on reproductive tissues: an overview from gametogenesis to gestation. Annals of Translational Medicine2(6), 55. http://doi.org/10.3978/j.issn.2305-5839.2014.06.04

Glueck, C. J., Goldenberg, N., Pranikoff, J., Khan, Z., Padda, J., & Wang, P. (2013). Effects of metformin-diet intervention before and throughout pregnancy on obstetric and neonatal outcomes in patients with polycystic ovary syndrome. Current Medical Research and Opinion29(1), 55–62. http://doi.org/10.1185/03007995.2012.755121

Neveu, N., Granger, L., St-Michel, P., & Lavoie, H. B. (2007). Comparison of clomiphene citrate, metformin, or the combination of both for first-line ovulation induction and achievement of pregnancy in 154 women with polycystic ovary syndrome. Fertility and Sterility87(1), 113–120. http://doi.org/10.1016/j.fertnstert.2006.05.069

Peat, R. (1997). From PMS to Menopause: Female Hormones in context.

http://raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml

Thatcher, S. S., & Jackson, E. M. (2006). Pregnancy outcome in infertile patients with polycystic ovary syndrome who were treated with metformin. Fertility and Sterility85(4), 1002–1009. http://doi.org/10.1016/j.fertnstert.2005.09.047