With ‘low carb’ diets continuing to be as popular as ever, read on to to find out whether there are any evidence-based uses for these diets. This article was first published in the November 2017 edition of NHD Extra.
The recommended daily intake of carbohydrates for the general public is around 50% of total dietary energy, which is roughly 313g of carbohydrates per day for the average man and 250g for the average woman1. Low carbohydrate diets (LCDs) involve eating less than 26% of your daily total calorie intake from carbohydrates1-2.
There are many variations of low carbohydrate diets and these can either be viewed as a fad or a valid clinical diet depending on the context.
Table 1: Classification of LCDs1-2
|Classification||Daily Carbohydrate Limit*||% of Daily Calorie Intake from Carbohydrates||Examples|
|Moderate carbohydrate diet||130 – 225g||26 – 45%||The Scarsdale Diet
The Zone Diet
|Less than 130g||Less than 26%||The Paleo Diet
The Drinking Man’s Diet
|Very-low carbohydrate diet||Less than 30g||Less than 6%||The Ketogenic Diet
The Atkins’ Diet
*Based on a 2000 kcal daily intake (the recommended daily calorie intake for a moderate active woman who weighs about 60kg)
Mechanism of LCDs
Limiting carbohydrate intake reduces the rate of insulin released from the pancreas and promotes glucagon secretion which causes3:
- Glycogenolysis: the breakdown of carbohydrate stored in liver and muscle tissue so that glucose can be used as an energy source
- Gluconeogenesis: creating new glucose (to be used as an energy source) using non carbohydrate sources such as certain amino acids, pyruvate, lactate and glycerol
- Lipolysis: the breakdown of fat into glycerol and free fatty acids
More extreme LCDs cause a type of fat burning called ketosis which is a compensatory mechanism usually occurring in starvation.
When glycogen stores are depleted, fatty acid oxidation can occur in the liver which produces ketones (or ketone bodies) which can be converted and used as an energy source. However, roughly 10 – 20% of ketone bodies are thought to be excreted via the skin, urine and breath without being metabolised3. Although ketosis can result in acidosis in a person who has diabetes, this is not usually seen to occur in starvation or carbohydrate restriction in those who don’t have diabetes3.
Epilepsy and Metabolic Disorders
The ‘ketogenic diet’ is a low carbohydrate, high fat diet which was developed in the 1920s to treat epilepsy in children.
This can still be used today under medical and dietetic guidance for children who don’t tolerate or don’t respond to epilepsy medication4-5. Although NICE supports this use of ketogenic diets, there is no official recommendation related to the treatment of adult epilepsy due to limited evidence6.
The ketogenic diet can also be used under medical and dietetic supervision with certain metabolic conditions such as: pyruvate dehydrogenase deficiency (PDH) and glucose transporter type 1 deficiency syndrome (GLUT1)4. The main types of ketogenic diets which are used in clinical practice are outlined in table 2 below.
Table 2: Variations of Ketogenic Diets
|Type of Diet||Diet Composition|
|The Classical Ketogenic Diet (KD)||A ratio of 3 – 4g of fat is given for every 1g of carbohydrate and protein7|
|The Modified Atkins Diet (MAD)||Restricts carbohydrates to 15 – 20g per day but doesn’t restrict protein and encourages fat intake8|
|The Low Glycemic Index Treatment (LGIT)||40 – 60g of carbohydrates are allowed per day (portion sizes are used as a guide), low GI options are encouraged, fats are encouraged and protein is unrestricted4, 9-10|
|The Medium Chain Triglyceride (MCT) Ketogenic Diet||60% of energy is derived from MCT fat, or a modified version to improve tolerance which has 30% MCT plus 30% from long chain fatty acids7|
Some meta-analysis’ have identified that LCDs resulted in more weight loss than other dietary methods11-12. Suggested reasons for this include: a loss of fluid as the process of breaking down glycogen stores can result in about 1kg weight loss as a result of fluid loss3,13 and a reduction in calories which may be partially due to the satiating effect of a high protein intake4, 14-15.
However, when SACN reviewed the overall evidence base in 2015 they concluded that energy restricted, high carbohydrate, low fat diets were more beneficial in reducing BMI when compared to LCDs1.
SACN’s (2015) also found no significant difference in energy intake when diets with different proportions of carbohydrates, protein and fat were compared1. Although sugar-sweetened drinks are associated with weight gain and a higher BMI in children and adolescents, when the total amount of carbohydrate was the diet was examined in this group, no association was found between carbohydrate intake and BMI or body fatness1.
Evidence is conflicting in terms of compliance when LCDs are compared with low fat diets15-16. However, for some individuals restricting the intake of a specific food group may increase the risk of binge eating and subsequent weight gain17.
Some studies have found an association between LCDs and improved glycemic levels18-19. But SACN (2015) found that “total carbohydrate intake appears to be neither detrimental nor beneficial to cardio-metabolic health” which included glycemia and incidence of type 2 diabetes1. More recently, Diabetes UK released a position statement which concluded that for Type 2 Diabetes LCDs can be safe and effective, but there is not enough evidence that this approach is better than others in terms of long term weight management and glycemic control and that “there is no strong evidence to say that [LCDs are] safe or effective for people with Type 1 diabetes”20. However there is ongoing research into carbohydrate intake and diabetes.
In terms of cardiovascular disease, some trials have identified an association between total carbohydrate intake and fasting blood lipids, and between carbohydrate intake and systolic blood pressure; however due to confounding factors such as weight loss is not possible to establish a causal relationship1. When different sources of carbohydrate are examined the associated cardiometabolic health outcomes vary (see table 3)1.
But overall SACN (2015) found that total carbohydrate intake had a neutral effect on cardiovascular disease endpoints1.
Table 3: Carbohydrate Sources and Cardiometabolic Health Associations (SACN 2015)1
|High intake of sugars-sweetened beverages||Increased risk of type 2 diabetes|
|Diet high in glycaemic index or glycaemic load||Increased risk of type 2 diabetes|
|High glycaemic load||Increased risk of cardiovascular disease|
|High intake of white rice||Increased risk of type 2 diabetes in certain Asian populations|
|Consuming brown rice||Reduced risk of type 2 diabetes|
|High intake of potatoes||Increased risk of type 2 diabetes – but it is not possible to establish a causal link due the confounding factors such as varied cooking methods (e.g. frying potatoes)|
|High intake of dietary fibre, cereal fibre and wholegrains||Reduced incidence of type 2 diabetes, cardiovascular disease, and coronary events|
|High intake of bran and beta-glucan||Lower total cholesterol, LDL cholesterol and blood pressure|
There is a hypothesis that ketogenic diets may be useful in combatting cancer which is based on ‘The Warburg Effect’; an observation that cancer cells prefer producing energy via anaerobic glycolysis rather than oxidative phosphorylation21. Although there are some animal and in vitro studies which support the use of the ketogenic diet with specific types of tumour cells22-24, there is also some contradictory research25 and other studies have identified that ketones may actually fuel certain cancer cells26-27.
Any advice for cancer patients to adopt this often restrictive diet needs to be underpinned by solid evidence; especially as this group are already at risk of malnutrition and cachexia.
Research is ongoing in this area, but currently more evidence is needed before the use of the ketogenic diet can be promoted as a routine treatment option for cancer21,28.
Although most people in the UK would benefit from reducing our intake of ‘free sugars’ (those added to foods by manufacturers, cooks or consumers, and the sugar found naturally in syrups, honey, syrups and unsweetened fruit juices), vilifying total carbohydrates intake can be harmful as it is recommend that 50% of dietary energy should come from carbohydrates1.
Carbohydrates are the main source of fuel used by our body and are also found in many nutritious foods such as: wholegrains, fruit, vegetables and dairy products1,26
For example there is strong evidence that fibre and wholegrains are associated with a lower risk of cardiovascular disease, diabetes and colorectal cancer1. Furthermore, a LCD may result in an increased intake of saturated fat and a high intake of saturated fat is is associated with an increased risk of cardiovascular disease29-30.
Considering that on average UK adults already consume less fibre and more saturated fat than the recommended level31, a LCD could potentially have an adverse nutritional effect.
There are some well-established clinical uses for LCDs, such as using ketogenic diets with certain metabolic disorders, or for seizure control in children with epilepsy which is unresponsive to medication. However, the current evidence is more conflicting in terms of weight management and cardiometabolic health. Although in the UK we should be aiming to reduce our intake free sugars, carbohydrates are also found in many nutritious foods. Therefore, LCDs should only be encouraged in specific situations when there is a clinical indication for their use.
- SACN (2015) “Carbohydrates and Health”
- Accurso et al. (2008) “Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal”
- Pogozelski et al. (2005) “The metabolic effects of low-carbohydrate diets and incorporation into a biochemistry course”
- GOSH website “Ketogenic Diet” (accessed July 2017: http://www.gosh.nhs.uk/health-professionals/clinical-guidelines/ketogenic-diet)
- Cross (2010) “Dietary therapies – an old idea with a new lease of life”
- The NICE (2017) “NICE Pathways – Epilepsy Overview”
- Neal et al. (2009) “A randomized trial of classical and medium-chain triglyceride ketogenic diets in the treatment of childhood epilepsy”
- Epilepsy Foundation “Modified Atkins Diet” (accessed July 2017: http://www.epilepsy.com/learn/treating-seizures-and-epilepsy/dietary-therapies/modified-atkins-diet)
- Epilepsy Foundation “The LGIT and the Keogenic DIet” (accessed July 2017: http://www.epilepsy.com/article/2007/5/low-glycemic-index-treatment-and-ketogenic-diet
- Matthew’s Friends “MAD & LGIT” (accessed July 2017: http://www.matthewsfriends.org/keto-therapies/keto-introduction/modified-ketogenic-diets-mad-lgit/)
- Mansoor et al. (2016) “Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of RCTs”
- Hession et al. (2008) “ Systematic review of RCTs of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities”
- Denke (2001) “Metabolic effects of high-protein, low-carbohydrate diets”
- Freedman et al. (2001) “Popular diets: A scientific review”
- Johnstone (1996) “Effect of overfeeding macronutrients on day-to-day food intake in man”
- Dyson et al. (2010) “An assessment of low-carbohydrate or low-fat diets for weight loss at 2 year’s follow-up”
- Blomquist & Grilo (2011) “Predictive Significance of Changes in Dietary Restraint in Obese Patients with Binge Eating Disorder During Treatment”
- Castaneda-Gonzalez et al. (2011) “Effects of low carbohydrate diets on weight and glycemic control among type 2 diabetes individuals: a systemic review of RCT greater than 12 weeks”
- Naude et al. (2014) “Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis”
- Marcias & Shapre (2017) “Assessing the Role of the Ketogenic Diet as a Metabolic Therapy in Cancer: Is it Evidence Based?”
- Stafford et al. (2010) “The ketogenic diet reverses gene expression patterns and reduces reactive oxygen species levels when used as an adjuvant therapy for glioma”
- Woolf et al. (2015) “The Ketogenic Diet Alters the Hypoxic Response and Affects Expression of Proteins Associated with Angiogenesis, Invasive Potential and Vascular Permeability in a Mouse Glioma Model”
- Woolf et al. (2016) “Tumor Metabolism, the Ketogenic Diet and β-Hydroxybutyrate: Novel Approaches to Adjuvant Brain Tumor Therapy”
- Rieger et al. (2014) “ERGO: A pilot study of ketogenic diet in recurrent glioblastoma”
- Martinez-Outschoorn et al. (2011) “Ketones and lactate increase cancer cell stemness”
- Bonuccelli et al. (2010) “Ketones and lactate ‘fuel’ tumor growth and metastasis”
- Erickson et al. (2017) “Systematic review: isocaloric ketogenic dietary regimes for cancer patients”
- Martinez-Outschoorn et al.(2012) “Ketone body utilization drives tumor growth and metastasis”
- NICE (2010) “Cardiovascular Disease Prevention”
- Hooper (2015) “Reduction in Saturated Fat Intake For Cardiovascular Disease”
- PHE (2016) “NDNS Results from Years 5 and 6 of the Rolling Programme (2012/2013 – 2013/2014)”