On April 18, 2019, the American Diabetes Association published a new Consensus Report which not only includes the use of a low carbohydrate eating pattern of 26-45% of total daily calories as carbohydrate, but in this report also includes the use of a very low carbohydrate (ketogenic) eating pattern of 20-50 g carbs per day. The report is clear that there is no “one-size-fits-all” eating pattern for the prevention or management of diabetes, and that it unrealistic to expect that there should be just one eating pattern for everyone; especially given the wide variety of people affected by diabetes and pre-diabetes, including their varied cultural backgrounds, personal preferences, co-occurring conditions and the variety of socio-economic backgrounds from which they come.
The new report underlines several eating patterns that are effective to varying degrees for achieving different goals, with potential benefits including HbA1C reduction, weight loss, lowered blood pressure, improved lipids (higher HDL-c, lower LDL-c), lower triglycerides (TG), but says clearly that low carb eating patterns show the most evidence for blood glucose control;
“Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia (blood sugar) and may be applied in a variety of eating patterns that meet individual needs and preferences.”
The new Consensus Report includes low carb eating patterns and very low carb (keto) eating patterns among the choices of eating patterns for those with pre-diabetes as well as adults with Type 1 or Type 2 Diabetes.
The various eating patterns with their different potential benefits are summarized in Table 3, below;
Table 3 – Eating Patterns reviewed for this report
The report also indicates that for adults with Type 2 Diabetes not meeting their blood sugar targets, or where there is a need to lower anti-glycemic medications that lower blood sugar, that
“reducing overall carbohydrate intake with low- or very low- carbohydrate eating plans is a viable approach.”
If you have been recently diagnosed as pre-diabetic or as having Type 2 Diabetes (T2D) and would like support to reverse the symptoms through a low carbohydrate or very low carbohydrate eating pattern, then I can help. I also don’t believe there is a “one-sized-fits-all” approach to either of these and will work within you needs to design an individual plan just for you.
You can learn more about my services including individual hourly appointments and sessions as well as packages above under the Services tab or in the Shop.
If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.
LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
Reference
Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
Yesterday, the headlines screamed out from around the world that a new study from Oxford University found that there is a 20% higher chance of developing colorectal cancer from eating as little as one strip of bacon per day. This sounds terrible, but is it true? To understand what this study is reporting, it is important to understand the difference between relative risk and absolute risk.
Absolute Risk
It was known before this study, that regardless what people eat, there is approximately a 5% chance of developing colorectal cancer in a person’s lifetime (whether they eat bacon every day or not). This is known as the absolute risk.
A 5% likelihood means that for every 100 people, 5 will get colorectal cancer regardless what they eat.
Illustrated, this looks as follows;
Absolute Risk: 5% = 5 per every 100 people
Relative Risk
The study reported that there is a20% higher chanceof developing colorectal cancer by eating as little as one strip of bacon per day.
This means that compared to not eating bacon daily, eating it daily results in one more person per 100 people developing colorectal cancer in their lifetime.
This is known as relative risk and illustrated that looks as follows:
20 % increase in relative risk
Headlines as click-bate
“People who ate 76 grams of red and processed meat per day — that’s in line with current guidelines and roughly the same as a quarter-pound beef burger — had a 20% higher chance of developing colorectal cancer compared to others, who ate about 21 grams a day” – https://www.cnn.com/2019/04/17/health/colorectal-cancer-risk-red-processed-meat-study-intl/index.html
It wasn’t only the American media that reported this, Canadian new outlet CTV did also.
“Scientists found that colorectal cancer risk rose 20 per cent with every 25 grams of processed meat people ate per day, equivalent to a strip of bacon or slice of ham.“ (https://www.ctvnews.ca/health/just-a-strip-of-bacon-a-day-increases-cancer-risk-u-k-study-finds-1.4383867)
Each individual person’s increased risk of getting colorectal cancer by eating as little as 1 strip of bacon per day is NOT 20%!Their increased absolute risk of getting colorectal cancer (*based on this study) is0.08%.
*this study was an epidemiological study, not a clinical study and can only show if there is an association between two factors and cannot make any conclusions about cause. The difference is explained below.
The study found that for every 10,000 people who ate 21g a day of red and processed meat, 40 were diagnosed with colorectal (bowel) cancer, and a single slice (or rasher) of bacon is ~23g.
i.e. 40 / 10,000 = 0.4%
The study also found that for every 10,000 people who ate 76g a day of red and processed meat, 48 were diagnosed with colorectal (bowel) cancer.
i.e. 48/10,000 = 0.48%
The actual chance of a person getting colorectal cancer (i.e. absolute risk)from eating bacon daily is the difference between these two numbers; i.e. 0.4% – 0.48% = 0.08%
Association is not Causation
This was an epidemiological study based on population data, and was not a clinical study.
Epidemiological studies are the study of diseases in populations and are helpful for researchers to know which areas warrant clinical studies.
It is important to know that epidemiological studies cannot attribute “cause” of disease or death. When an epidemiological study finds an “association” between two factors such as bacon and higher colon cancer rates — this does NOT mean that eating bacon ’causes’ heart disease.
Based on this study, all that can be said is that there was an increase in the association between eating bacon and absolute rates of colon cancer of 0.08%.
Not so impressive now, is it?
If you are having trouble sifting through all the information you read and in knowing if it is accurate, or even says what it seems to be saying, I can help. Sometimes people start by booking an appointment just to ask me those types of questions, because they want credible answers.
You can learn more about my services including individual hourly appointments and sessions as well as packages above under the Services tab or in the Shop.
If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.
LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
Reference
Kathryn E Bradbury, Neil Murphy, Timothy J Key, Diet and colorectal cancer in UK Biobank: a prospective study, International Journal of Epidemiology, , dyz064, https://doi.org/10.1093/ije/dyz064
A newly published large-scale epidemiological study has reported that taking vitamin and mineral supplements does not reduce the risk of cardiovascular disease such as heart attack and stroke, cancer rates or other causes of health-related death. The study published Tuesday, April 9, 2019 in the Annals of Internal Medicine analyzed US nutritional data from 30, 899 adults over the age of twenty from the NHANES survey between 1999 to 2010 and linked it to mortality data from the National Death Index [1]. During the six year follow-up period there were 3613 deaths; of which 945 were cardiovascular-related and 805 were from cancer.
Vitamin and Mineral Supplement versus Nutrient Intake from Food
The study found that use of vitamin and mineral supplements was not related to improved outcomes in rates of death from cardiovascular disease, cancer or all-cause health related death. Adequate intake of vitamin A, vitamin K, magnesium, zinc and copper was associated with reduced rates of cardiovascular disease and death from all health-related causes, but these improved associations only applied to those who obtained these nutrients from food.
Calcium Supplements – too much of a ‘good’ thing
So many adults take calcium supplements, however calcium intake from supplements of ≥ 1000 mg/day (which many adults take!) was associated with increased risk of death from cancer.
Want to Live Longer? Eat Whole, Real Food
Based on this large-scale epidemiological study, eating foods rich in vitamin A, vitamin K, magnesium, zinc and copper was associated with reduced rates of cardiovascular (CVD) disease and death from all health-related causes. Good news! All of these nutrients are widely available in whole, real foods that also happen to be low in carbohydrate.
Zinc and Copper
Meat and seafood are some of the richest sources of zinc and copper.
Vitamin K
Dark, leafy greens are excellent sources of vitamin K. Vitamin K is needed to help the body absorb vitamin D and to help with proper calcium utilization.
Magnesium
Nuts and seeds, including cocoa beans (think ‘dark chocolate’!) are very good sources of magnesium, as are avocados
Vitamin A
…and yellow and orange vegetables are excellent sources of vitamin A.
Final thoughts…
Epidemiological studies (which are the study of diseases in populations) are helpful to know what areas warrant good quality clinical trials, but aren’t useful for attributing “cause” of disease or death. When an epidemiological study finds an “association” between two factors, this does NOT mean that one causes the other. For that, clinical trials are necessary. That said, eating whole, real foods that also happen to be low in carbohydrate are an excellent way to get all of the nutrients that this study found are associated with lower rates of cardiovascular disease and death from all health related causes and it is pretty difficult to eat too much of any nutrient when eating whole, real food. Since taking vitamin and mineral supplements is not associated with lower rates of disease or death, and in the cases of calcium supplements may even be associated with negative health outcomes, eating a whole-food diet rich in the above foods is the safest way to ensure adequate intake of these nutrients. If you would like more information about how much of these foods you should be eating, I’d be glad to help. Please have a look at the Services tab or the Shop for more information. To your good health! Joy You can follow me on:
Chen F, Du M, Blumberg JB, Ho Chui KK, Ruan M, Rogers G, et al. Association Among Dietary Supplement Use, Nutrient Intake, and Mortality Among U.S. Adults: A Cohort Study. Ann Intern Med. [Epub ahead of print ] doi: 10.7326/M18-2478
Note: This article was originally posted on April 9, 2019, and was updated and reposted on November 9, 2025.
Introduction
Did you know that “complex carbohydrates” are just long chains of sugar molecules, like pearls on a string? How quickly and how high blood sugar spikes depend on what those sugars are.
This article was inspired by a graphic shared by Dr. RD Dikeman* on social media (in 2019), which shows complex carbohydrates as long chains of glucose — exactly what starches are. Not all complex carbohydrates are simply glucose chains; some are composed of other sugars and can affect blood sugar levels differently. This article explains: 1. What complex carbohydrates are 2. How they are digested 3. How different types affect blood glucose.
graphic from RD Dikeman, Typeonegrit
*Dr. RD Dikeman holds a PhD in Theoretical and Mathematical Physics and became highly knowledgeable about carbohydrate metabolism after his son was diagnosed with Type 1 Diabetes in 2013. At that time, his son was eating 40–60 grams of carbohydrates per meal and experienced large swings in blood sugar, including an episode of ketoacidosis — a dangerous condition caused by very high ketone levels due to insufficient insulin. This is different from ketosis, which is a normal state when the body uses fat for energy, such as after an overnight fast. About five years ago, Dr. Dikeman’s son began following the low-carbohydrate protocol outlined in Dr. Richard Bernstein’s book Diabetes Solution. Since then, he has been able to maintain stable blood sugar levels with the minimum necessary insulin doses.
I liked the analogy of Dr. Dikeman’s graphic and wanted to use it as a ‘jumping off point’ for this article.
Glucose — Explained Simply
Glucose (also called dextrose) is the main sugar in your blood. That’s why blood sugar and blood glucose mean the same thing. Glucose is one of two main energy sources — the other is ketones. Even people who don’t eat low-carb diets make small amounts of ketones after a night’s sleep. The body uses both glucose and ketones for energy. Carbohydrate-containing foods are broken down into glucose for energy; however, the body can also produce glucose from protein and fat through gluconeogenesis, ensuring that the brain and red blood cells always have glucose [1].
The Glucose–Complex Carb Analogy
In Dr. Dikeman’s illustration, complex carbohydrates are shown as long chains of glucose molecules — like a string of pearls. Starches are long chains of glucose; however, not all complex carbohydrates are composed of only glucose. Some carbohydrates include other simple sugars such as galactose or fructose, which the body digests differently. Other complex carbohydrates (like some fibers and oligosaccharides) contain mixed sugars that may or may not be digestible [1][2].
Simple vs. Complex Carbohydrates
Carbohydrates are often divided into simple sugars, which consist of one or two sugar molecules, and complex carbohydrates, which are made up of three or more sugar molecules linked together.
Simple Sugars
Monosaccharides
Simple sugars are called monosaccharides (“mono” means one) because they are made from a single sugar molecule.
Examples: glucose, fructose, galactose.
Disaccharides
Disaccharides are also simple sugars (“di” means two). They are two sugar molecules joined together.
Examples:
Sucrose = glucose + fructose
Lactose = glucose + galactose
Maltose = glucose + glucose
Simple sugars (monosaccharides) such as glucose break down much more quickly and, as a result, have a much quicker impact on blood sugar than disaccharides (made up of two sugar molecules) like sucrose (table sugar).
Complex Carbohydrates
Complex carbohydrates are made up of three or more sugar molecules linked together.
Oligosaccharides contain 3–10 sugar molecules and are found in beans, peas, and lentils.
Humans cannot digest oligosaccharides; however, our gut bacteria can ferment [1][5].
Polysaccharides contain hundreds or thousands of sugar molecules. When all sugars are glucose, the polysaccharide is called starch. Polysaccharides that humans cannot digest, such as cellulose and hemicellulose, are fiber, which slows digestion and can help control blood sugar [1].
Starch
Starches are long chains of glucose molecules, strung together like a string of pearls. They are found in grains, including wheat, corn, rice, oats, millet, and barley, as well as tubers such as potatoes, yams, sweet potatoes, and cassava.
There are two types of starches: the long unbranched chains called amylose and the long branched chain ones called amylopectin.
Amylopectin is digested more easily than amylose. Cornstarch, high in amylopectin, digests faster than wheat starch, which has more amylose [1].
Since each “pearl” on the string is glucose, which is a simple, quickly absorbed monosaccharide, digestion of these starches occurs quickly, and so does the corresponding spike in blood sugar. Enzymes act to cut the connection between the glucose molecules (i.e., the “pearls”), and that “complex carbohydrate” becomes many individual simple sugar molecules.
Digestion of Carbohydrates
Digestion of carbohydrates begins in the mouth. This is where salivary amylase starts breaking starch into smaller polysaccharides and maltose. The process continues in the stomach, where the high acid environment temporarily halts digestion, then continues in the small intestine, where pancreatic amylase breaks starch into maltose (two glucose molecules). Fo
Brush-border enzymes split maltose into two glucose molecules. The enzymes sucrase and lactase split sucrose and lactose into glucose, fructose, and galactose [1][3].
Monosaccharides are absorbed into the small intestine and transported to the liver, where fructose and galactose are converted to glucose, then stored in the liver as glycogen. When glycogen stores are full, excess glucose is converted to fat [1][2]. These are quickly absorbed and, as a result, have the most immediate effect on blood sugar.
Carbohydrates and Type 2 Diabetes
As covered in previous articles, including this one, there is no requirement for people to eat carbohydrate-based food provided that adequate amounts of protein and fat are consumed [3]. In the absence of carbohydrates in the diet, fats and proteins can be used by the body to produce glucose for the brain, in a process called gluconeogenesis. This does not mean that I recommend people avoid eating carbohydrate-based food, but rather to be aware of how carbs affect their blood sugar.
People with type 2 diabetes or pre-diabetes should monitor the effect that carb-based foods have on their blood sugar. Some people do well eating legumes (pulses), including whole (not pureed) black beans, white navy beans, pinto beans, red and white kidney beans, chickpeas, and fava beans [5] because the fiber in them slows down their digestion. The reason pureed legumes have a very different effect on blood sugar than whole, cooked legumes is covered in this earlier article, under the header “The Effect of Mechanical Processing on Blood Glucose Response”.
The effect of simple sugars and starches on blood sugar is very different, because they are simply a string of “pearls”, where the pearls are glucose and easily split during digestion.
Personalized nutrition is key. “Eating to your meter” helps those with type 2 diabetes test how specific foods affect their blood sugar [4].
Final Thoughts
Carbohydrates are just strings of pearls, where the pearls are sugar molecules. Starches are made up of only glucose molecules, which are easily split apart during digestion, resulting in large amounts of individual glucose molecules that quickly spike blood sugar.
Legumes (pulses, beans) eaten whole (not pureed, which speeds up their digestion and results in a spike in blood sugar) and in small portions are digested more slowly and less likely to spike blood sugar. Monitoring the effect of food on blood sugar is essential for those with type 2 diabetes or those with pre-diabetes and for those at risk.
Personalized nutrition focuses on customizing your diet — the types of foods, portion sizes, and timing — to meet your specific health needs, and it is at the heart of the routine services that I offer.
For more information, please visit the Services tab above.
Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015;163(5):1079-1094. [https://pubmed.ncbi.nlm.nih.gov/26590418/]
Sievenpiper JL, Kendall CWC, Esfahani A, et al. Effect of non-oil-seed pulses on glycaemic control: systematic review and meta-analysis. Diabetologia. 2009;52:1479. [https://pubmed.ncbi.nlm.nih.gov/19526214/]
LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, as well as all other material contained here (the ”content”), are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis, and/or treatment. It is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
A recently published meta-analysis of 43 cohort or nested case-control studies up until July 1, 2018 [1] did not find that higher saturated fat intake is associated with higher risk of cardiovascular disease (CVD) events. This is the first study to examine the effect of total dietary fat intake and the intake of specific fatty acids on CVDs risk based on dose-response meta-analysis of prospective cohort studies.
It has been proposed that saturated fat (SFA) and trans fatty acids (TFA) contribute to CVD via inflammatory mechanisms and oxidative stress, mediated through the production of reactive oxygen species (ROS) [2,3]. With respect to trans fatty acids, this new study found that dietary TFA intake had a dose-response association with CVDs risk; specifically a 16% increased risk of CVD with an increased TFA intake of 2% of energy per day, however no association was observed between total fat or dietary saturated fatty acid (SFA) intake and the risk of CVDs [1]. In addition, this meta-analysis found no protective effect from the consumption of either monounsaturated fatty acids (MUFA), or polyunsaturated fatty acids (PUFA) and risk of CVDs, except PUFAs showed a protective effect in sub-group analysis followed up for more than 10 years [1].
These findings do not support 2010 recommendations of the WHO / FAO [4] which continue to influence national dietary guidelines around the world to recommend reducing intake of saturated fat in order to lower the rates of CVD.
As well, these new findings call into question the findings of the PREDIMED study [5] and the Lipid Research Clinics Prevalence Follow-up Study [6] that indicate that diets high in polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) and low in saturated fatty acid (SFA) and trans fatty acids (TFA) are associated with reduced CVDs events.
The authors caution that;
“it is possible that the role of dietary fat played in the development of CVDs might be confounded by the fat sources. For instance, vegetables and fruits play protective roles in the development of CVDs. However, we could not investigate the different effects of fat from animal, vegetables and fruit separately in this current meta-analysis.” [1]
Some thoughts…
For almost 50 years it has been believed that dietary saturated fat intake was a risk factor for CVDs based on the assumption that dietary fat can increase low density lipoprotein (LDL) cholesterol and blood pressure and in turn, increase CVDs risk, however this meta-analysis of 43 cohort studies did not find a positive association between total dietary fat intake or saturated fat intake and CVDs risk.
The 2017 Prospective Urban Rural Epidemiological (PURE) study (covered in this earlier article) is the only prospective study to date which covered multiple world regions and which found that total dietary fat and types of dietary fat were not associated with cardiovascular disease or mortality and further, that dietary saturated fat had an inverse association with stroke and a risk of all-cause mortality with higher intake (up to ~14% of energy intake). That is, dietary saturated fat intake was protective.
The findings of the current meta-analysis study, combined with the findings of the 2017 PURE study call into question current dietary recommendations which continue to recommend that people limit dietary saturated fat in order to reduce cardiovascular risk. Such recommendations are included in the most recent Canada’s Food Guide which encourages Canadians to ”choose foods with healthy fats instead of saturated fat” and to ”prepare meals and snacks using ingredients that have little to no added sodium, sugars or saturated fat” (see this article for details) .
Post publication note (April 7, 2019): As I’ve stated in previous articles, I am not opposed to Canada’s new Food Guide. It is a huge improvement over it’s predecessor for many reasons already discussed. My two concerns that I’ve expressed previously remain; (a) that the recommendations for the general population to continue to limit saturated fat because it contributes to CVD has not been conclusively demonstrated. The only thing that has been shown is that saturated fat can raise LDL, but which LDL; the large fluffy sub-fraction, or the small dense sub-fraction? Please see article linked to above for an elaboration. My second concern is that; (b) the amount of carbohydrate in the diet is too high for the large percentage of the population that are metabolically unhealthy. Please see this article for an elaboration.
Author’s Conclusions
The study’s authors concluded that;
“This current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion. Furthermore, the subgroup analysis found a cardio-protective effect of PUFA in studies followed up for more than 10 years. Dietary guidelines taking these findings into consideration might be more credible.” [1]
If you would like to learn about the types of fats in your diet and how they may impact your health or those of your family, please send me a note through the Contact Me form on the tab above. You can learn more about the services I provide by clicking on the Services tab or having a look in the Shop.
LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
References
Zhu Y, Bo Y, Liu Y, Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies, Lipids in Health and Disease (2019) 18:91, https://doi.org/10.1186/s12944-019-1035-2
Sverdlov AL, Elezaby A, Qin F, Behring JB, Luptak I, Calamaras TD, Siwik DA, Miller EJ, Liesa M, Shirihai OS, et al. Mitochondrial reactive oxygen species mediate cardiac structural, functional, and mitochondrial consequences of diet-induced metabolic heart disease. J Am Heart Assoc. 2016;5:e002555.
Ruparelia N, Chai JT, Fisher EA, Choudhury RP. Inflammatory processes in cardiovascular disease: a route to targeted therapies. Nat Rev Cardiol. 2017;14:133—44.
Nations FaAOotU. Summary of conclusions and dietary recommendations on total fat and fatty acids in fats and fatty acids in human nutrition—report of an expert consultation. Geneva: FAO/WHO; 2010.
Estruch R, Ros E, Salas-Salvado J, Covas MI, Corella D, Aros F, Gomez- Gracia E, Ruiz-Gutierrez V, Fiol M, Lapetra J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279—90.
Guasch-Ferre M, Babio N, Martinez-Gonzalez MA, Corella D, Ros E, Martin-Pelaez S, Estruch R, Aros F, Gomez-Gracia E, Fiol M, et al. Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease. Am J Clin Nutr. 2015;102:1563—73.
Dehghan M, Mente A, Zhang X, Swaminathan S, Li W, Mohan V, Iqbal R, Kumar R, Wentzel-Viljoen E, Rosengren A, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017;390:2050—62.
