I'm a Biomedical Scientist with expertise in lipid metabolism, nutritional biochemistry and cardiovascular disease. After gaining a BSc with first class honours in medical laboratory science at Portsmouth Polytechnic in 1984, I undertook a PhD on the effects of exercise and diet on human plasma lipoproteins at the University of Aberdeen, under the supervision of Professor Ronald Maughan and Dr Roy Skinner (1988). This was followed by postdoctoral research in Pathological Biochemistry at Glasgow Royal Infirmary with Professors Jim Shepherd and Chris Packard.
Since 1994, I've held academic posts as a Lecturer, Senior Lecturer, Reader and Professor of Nutritional Metabolism at the University of Surrey. I teach undergraduate dietitians, nutritionists and food scientists, as well as nutritional medicine and human nutrition masters students.
I'm an active researcher and external speaker in human nutrition, in relation to cardiovascular health, and I've published widely in the areas of blood lipids, dietary macronutrients and cardiovascular disease. My research has been supported by grants from the Medical Research Council, British Heart Foundation, Department for Environment Food and Rural Affairs, Food Standards Agency, Biotechnology and Biological Sciences Research Council, and various industries.
Areas of specialism
Affiliations and memberships
Business, industry and community links
- Chairman for the Exam Board in Nutritional Medicine 2006 to date
- Degree programme review panel member for BSc Undergraduate Framework for Lifelong Learning in Health and Social Care Practice, EIHMS, University of Surrey (2007)
- Member of the Faculty's Research Advisory Board, FHMS, University of Surrey (2014-16)
Impact of diet and lifestyle on the development and management of cardiovascular diseases, with a research focus on the effects of dietary macronutrients (fatty acids, sterols, carbohydrates, proteins) on cardio-metabolic risk factors associated with obesity, metabolic syndrome and type-2 diabetes.
Other specialisms include:
- The metabolism of serum lipid and lipoproteins (clinical lipidology),
- Cholesterol homeostasis
- Metabolic phenotypes (metabotypes)
- Nutrient-gene-environment interactions
- Personalised nutrition.
- University of Reading
- Kings College London
- Imperial College London
- MRC unit of Human Nutrition Research, Cambridge
- University of Glasgow
- Harakopio University, Athens, Greece
- Aarhus University, Denmark
Indicators of esteem
I am Research Section Leader in Metabolic Medicine, Food and Macronutrients within the Department of Nutritional Sciences at the University of Surrey.
Theme Leader in Whole Body Metabolism and member of the Scientific Committee for the Nutrition Society
Editorial Board Member for the European Journal of Nutrition
- 1991: Susceptibility of LDL subfractions to oxidative modification in relation to coronary heart disease. (MRC)
- 1991: Role of antioxidants and dietary fatty acids in the oxidative modification of human plasma LDL (MAFF)
- 1993: Low density lipoprotein carbohydrate as a determinant of LDL subfraction metabolism (MRC)
- 1996: Can the metabolic effects of dietary n-3 PUFA be explained by changes in the expression of lipase genes in adipose tissue? (BBSRC)
- 1997: The influence of dietary n-3 PUFA on the structure, function and metabolism of TAG-rich lipoproteins in healthy individuals. (BBSRC)
- 1998: Importance of alpha-linolenic acid as a source of long chain n-3 PUFA and its influence on risk factors of cardiovascular disease. (UK Food Standards Agency)
- 2000: Vitamin E biokinetics and metabolism in dyslipidaemia.(BHF)
- 2000: Quantification of the optimal n-6 / n-3 ratio in the UK diet. The 'OPTILIP' study (UK Food Standards Agency)
- 2003: Effect of low glycaemic index foods on blood lipids in type 2 diabetes
- 2003: Impact of the amount and composition of dietary fat and carbohydrate on metabolic syndrome and CVD risk; The 'RISCK' Study. (UK Food Standards Agency)
- 2005: Effects of increased egg consumption on a weight-reducing diet on blood cholesterol & related biomarkers of CHD risk (British Egg Information Service)
- 2008: Dietary intervention study to determine the effects of prawns on serum cholesterol and related biomarkers of CHD risk (DEFRA)
- 2009: How does dietary carbohydrate influence the formation of an atherogenic lipoprotein phenotype? (BBSRC)
- 2014: Risk-assessed exercise and diet intervention for men with prostate cancer. (Prostate Cancer UK)
- 2016: Mechanisms to explain variation in the serum low density lipoprotein cholesterol response to dietary saturated fat. (BBSRC)
Umpleby M, Shojaee-Moradie F, Fielding B, Li X, Marino A, Alsini N, Isherwood C, Jackson N, Ahmad A, Stolinski M, Lovegrove JA, Johnsen S, Jeewaka R Mendis AS, Wright J, Wilinska ME, Hovorka R, Bell JD, Thomas EL, Frost GS, Griffin BA (2017). Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets. Clinical Science 131, 2561-2573,
Cold F, Kristian HW, Pastor-Barriuso R, Rayman MP, Guallar E, Nybo M, Griffin BA, Stranges S, Cold S (2015). Randomised controlled trial of the effect of long-term selenium supplementation on plasma cholesterol in an elderly Danish population. British Journal of Nutrition 114, 1807-1818.
Johns I, Goff L, Bluck LJ, Griffin BA, Jebb SA, Lovegrove JA, Sanders TA, Frost G, Dornhorst A (2014) Plasma free fatty acids do not provide the link between obesity and insulin resistance or β-cell dysfunction: results of the ‘RISCK’ study. Diabetes Medicine 31,1310-1315.
Harman NL, Griffin BA, Davies IG (2013) Separation of the principal HDL subclasses by iodixanol ultracentrifugation. Journal of Lipid Research 54, 2273-2281.
Meyer BJ, Stewart FM, Brown EA, Cooney J, Nilsson S, Olivecrona G, Ramsay JE, Griffin BA, Caslake MJ, Freeman DJ (2013). Maternal obesity is associated with the formation of small dense LDL and hypo-adiponectinaemia in the third trimester. Journal of Clinical Endocrinology & Metabolism 98, 643-652.
Goff LM, Griffin BA, Lovegrove JA, Sanders TA, Jebb SA, Bluck LJ, Frost GS (2013). Ethnic differences in beta-cell function, dietary intake and expression of the metabolic syndrome among UK adults of South Asian, black African-Caribbean and white-European origin. Diabetes Vascular Disease Research 10, 315-323.
Fallaize R, Wilson L, Gray J, Morgan LM, Griffin BA (2012). Variation in the effects of three different breakfast meals on subjective satiety and subsequent intake of energy at lunch and evening meal. European Journal of Nutrition 52,1353-1359.
Fava F, Gitau R, Griffin BA, Tuohy KM, Gibson GR, Lovegrove JA (2012). Impact of the amount and quality of dietary fat and carbohydrate on the faecal microbiome and short-chain fatty acid excretion in a population “at-risk” of the metabolic syndrome. International Journal of Obesity 37, 216-223.
Walker CG, Loos RJF, Mander AP, Jebb SA, Frost GS, Griffin BA, Lovegrove JA, Sanders TAB and Bluck LJ (2012). Genetic predisposition to type 2 diabetes is associated with impaired insulin secretion but does not modify insulin resistance or secretion in response to an intervention to lower dietary saturated fat. Genes & Nutrition 7, 529-536.
AlSaleh A, Frost GS, Griffin BA, Lovegrove JA, Jebb SA, Sanders TAB and O’Dell SD on behalf of the RISCK Study investigators. (2012). PPARγ2 gene Pro12Ala and PPARα gene Leu162Val SNPs interact with dietary intake of fat in determination of plasma lipid concentrations. Journal of Nutrigenetics & Nutrigenomics 4, 354-366.
AlSaleh A, O’Dell SD, Frost GS, Griffin BA, Lovegrove JA, Jebb SA, Sanders TAB on behalf of the RISCK Study investigators (2011). Interaction of PPARG Pro12Ala with dietary fat influences plasma lipids in subjects at cardiometabolic risk. Journal of Lipid Research 52, 2298-303.
Rayman MP, Stranges S, Griffin BA, Pastor-Barriuso R, Guallar E (2011). Effect of supplementation with high-selenium yeast on plasma lipids: a randomized, controlled trial. Annals of Internal Medicine 154, 656- 665.
Walker CG, Goff L, Bluck LJ, Griffin BA, Jebb SA, Lovegrove JA, Sanders TA, Frost GS; on behalf of the RISCK Study Group (2011). Variation in the FFAR1 Gene Modifies BMI, Body Composition and Beta-Cell Function in Overweight Subjects: An Exploratory Analysis. PLoS One. 6: e19146.
Alsaleh A, O'Dell SD, Frost GS, Griffin BA, Lovegrove JA, Jebb SA, Sanders TA; on behalf of the RISCK Study Group (2011). Single nucleotide polymorphisms at the ADIPOQ gene locus interact with age and dietary intake of fat to determine serum adiponectin in subjects at risk of the metabolic syndrome. American Journal of Clinical Nutrition 94, 262-269.
Walker CG, Loos RJ, Olson AD, Frost GS, Griffin BA, Lovegrove JA, Sanders TA, Jebb SA (2011). Genetic predisposition influences plasma lipids of participants on habitual diet, but not the response to reductions in dietary intake of saturated fatty acids. Atherosclerosis 215, 421-427.
Toft-Petersen AP, Tilsted HH, Aaroe J, Rasmussen K, Christensen T, Griffin BA, Aardestrup, Andreasen A & Schmidt EB (2011). Small dense LDL particles - a predictor of coronary artery disease evaluated by invasive and CT-based techniques. Lipids in Health and Disease 10, 21.
Jebb SA, Lovegrove JA, Griffin BA, Frost GS, Moore CS, Chatfield MD, Bluck LJ, Williams CM, Sanders TAB (2010). Effect of changing the amount and type of fat and carbohydrate on insulin sensitivity and cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) Trial. American Journal of Clinical Nutrition 92, 748-758.
Isherwood C, Wong M, Jones WS, Davies IG, Griffin BA (2010). Lack of effect of cold water prawns on plasma cholesterol and lipoproteins in normo-lipidaemic men. Cellular and Molecular Biology 56, 52-58.
Hampton SM, Isherwood C, Kirkpatrick VJ, Lynne-Smith AC, Griffin BA (2010).The influence of alcohol consumed with a meal on endothelial function in healthy individuals. Journal of Human Nutrition & Dietetics 23, 120-125.
Moore C, Gitau R, Goff L, Lewis FJ, Griffin MD, Chatfield MD, Jebb SA, Frost GS, Sanders TAB, Griffin BA, Lovegrove JA (2009) Successful manipulation of the quality and quanity of fat and carbohydrate consumed by free-living individuals using a food exchange model. The Journal of Nutrition 139, 1534-1540.
Rasmussen JG, Eschen RB, Aardestrup IV, Dethlefsen C, Griffin BA, Schmidt EB (2009). Flow mediated vasodilation: variation and inter-relationships with plasma lipids and lipoproteins. Scandinavian Journal of Clinical laboratory Investigation 69, 156-160.
Harman NL, Leeds AR & Griffin BA (2008). Increased dietary cholesterol does not increase plasma low density lipoprotein when accompanied by an energy-restricted diet and weight loss. European Journal of Nutrition 47, 287-293
Lloyd DAJ, Paynton SE, Bassett P, Mateos AR, Lovegrove JA, Gabe SM & Griffin BA (2008). Assessment of long chain n-3 polyunsaturated fatty acid status and clinical outcome in adults receiving home parenteral nutrition. Clinical Nutrition 27, 822-831
Morgan LM, Griffin BA, Millward DJ, DeLooy A, Fox KR, Baic S, Bonham MP, Wallace JMW, MacDonald I, Taylor MA & Truby H (2008). Comparison of the effects of four commercially available weight loss programmes on lipid-based cardiovascular risk factors. Public Health Nutrition 23, 1-9.
Paschos GK, Zampelas A, Panagiotakos DB, Katsiougiannis S, Griffin BA, Votteas V & Skopuli F (2007). Effects of flaxseed oil supplementation on plasma adiponectin levels in dyslipidemic men. European Journal of Nutrition. 46, 315-320.
Khodadadi I, Griffin B, Thumser A (2007). Differential effects of long-chain fatty acids and clofibrate on gene expression profiles in cardiomyocytes. Archives of Iranian Medicine 11, 42-49.
Griffin MD, Sanders TAB, Davies IG, Morgan L, Millward DJ, Lewis F, Slaughter S, Cooper J & Griffin BA (2006). The effects of altering the ratio of dietary n-6/n-3 fatty acids on insulin sensitivity, lipoprotein size and postprandial lipemia in men and women aged 45 to 75 years, The OPTILIP study. American Journal of Clinical Nutrition 84, 1290-1298.
Sanders TAB, Lewis F, Slaughter S, Griffin BA, Griffin MD, Davies IG, Millward DJ, Cooper JA & Miller G. (2006). Effect of varying the ratio of n-6 to n-3 fatty acids by increasing the dietary intake of α-linolenic acid, EPA and DHA, or both on fibrinogen and clotting factors VII and XII in persons aged 45-70. The OPTILIP study. American Journal of Clinical Nutrition 84, 513-522.
Sanders TAB, Gleason K, Griffin BA & Miller GJ (2006) Influence of an algal triacylglycerol containing docosahexaenoic acid (22:6 n-3) and docosapentaenoic acid (22: 5 n-6) on cardiovascular risk factors in healthy men and women. British Journal of Nutrition. 95, 525-531.
Wilkinson P, Leach C, Ah-Sing E, Hussein N, Miller GJ, Millward DJ & Griffin BA (2005). Influence of a-linolenic acid and fish-oil on markers of cardiovascular risk in subjects with an atherogenic lipoprotein phenotype. Atherosclerosis 181, 115-124.
Panagiotakos DB, Pitsavos C, Zampelas A, Chrysohoou C, Griffin BA, Stefanadis C & Toutouzas P. (2005). Fish consumption and the risk of developing acute coronary syndromes: the CARDIO2000 study. International Journal of Cardiology 102, 403-409.
Paschos GK, Yiannakouris N, Rallidis LS, Davies I, Griffin BA, Panagiotakos DB, Skopouli FN, Votteas V, & Zampelas A. (2005) Apolipoprotein E-genotype in dyslipidaemic patients and response of blood lipids and inflammatory marker to a-linolenic acid. Angiology 56, 49-60.
Hussein N, Ah-Sing E, Wilkinson P, Leach C, Griffin BA & Millward DJ (2005). Relative rates of long chain conversion of [13C] linoleic and a-linolenic acids in response to their high and low dietary intakes in men with an atherogenic lipoprotein phenotype. Journal of Lipid Research 46, 269-280.
Davies IG, Graham JM & Griffin BA (2003). Rapid separation of LDL subclasses by iodixanol gradient ultracentrifugation. Clinical Chemistry 49, 1865-1872.
Khan S, Minihane AM, Talmud PJ, Wright JW, Murphy MC, Williams CM & Griffin BA (2002). Dietary long chain n-3 PUFAs increase LPL gene expression in adipose tissue of subjects with an atherogenic lipoprotein phenotype. Journal of Lipid Research 43, 979-985.
Leigh-firbank EC, Minihane A-M, Leake DS, Wright JW, Murphy MC, Griffin BA & Williams CM (2002). Eicosapentaenoic acid and docosahexaenoic acid from fish oils: differential associations with lipid responses. British Journal of Nutrition 87, 435-445.
Minihane AM, Khan S, Leigh Firbank E, Talmund PJ, Wright J, Murphy MC, Griffin BA & Williams CM (2000). Apo E polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype (ALP) Arteriosclerosis, Thrombosis & Vascular Biology 20, 1990-1997.
Griffin BA, Furlonger N & Iversen SA (2000). Plasma apolipoprotein B to low-density lipoprotein cholesterol ratio as a marker of small, dense low-density lipoprotein. Annals of Clinical Biochemistry 37, 537-539.
Minihane AM, Khan S, Williams DL, Wright JW, Murphy MC, Griffin BA & Williams CM (2000). In subjects with an atherogenic lipoprotein phenotype (ALP), central adiposity is associated with an attenuated post-prandial triglyceride response International Journal of Obesity 24, 1097-1106.
Griffin BA, Minihane AM, Furlonger N, Chapman C, Murphy M, Williams D, Wright JW, Williams CM. (1999). Inter-relationships between small, dense LDL, plasma triglyceride and LDL apoprotein B in an atherogenic lipoprotein phenotype (ALP) in free-living subjects. Clinical Science 97, 269-276.
Nigdikar SV, Williams NR, Griffin BA & Howard AN. (1998). Consumption of red wine polyphenols reduces the susceptibility of low-density lipoproteins to oxidation in volunteers. American Journal of Clinical Nutrition 68, 258-265.
Freeman DJ, Caslake MJ, Griffin BA, Hinnie J, Tan CE, Watson TDG, Packard CJ & Shepherd J. (1998). The effect of smoking on post-heparin lipoprotein and hepatic lipase, cholesteryl ester transfer protein and lecithin:cholesteryl acyl transferase activities in human plasma. European Journal of Clinical Investigation 28, 584-591.
Gaw A, Packard CJ, Lindsay GM, Murray EF, Griffin BA, Caslake MJ, Colquhoun I, Wheatley DJ, Lorimer AR & Shepherd. (1996). Effects of colestipol alone and in combination with simvastatin on apolipoprotein B metabolism. Arteriosclerosis, Thrombosis & Vascular Biology 16, 236-249.
Anber V, Griffin BA, McConnell M, Packard CJ & Shepherd J. (1996). Influence of plasma lipid and LDL-subfraction profile on the interaction between low density lipoprotein with human arterial wall proteoglycans. Atherosclerosis 124 (2), 261-271.
Tan KCB, Cooper MB, Ling KL, Griffin BA, Freeman DJ, Packard CJ, Shepherd J, Hales N & Betteridge DJ. (1995). Fasting and postprandial determinants for the occurrence of small, dense LDL species in non-insulin dependent diabetic patients with and without hyper-triglyceridaemia: the involvement of insulin, insulin precursor species and insulin resistance. Atherosclerosis 113, 273-287.
Gaw A, Packard CJ, Lindsay GM, Griffin BA, Caslake MJ, Lorimer AR & Shepherd J. (1995). Overproduction of small, very low density lipoproteins (Sf 20-60) in moderate hyper- cholesterolaemia: relationships between apolipoprotein B kinetics and plasma lipoproteins. Journal of Lipid Research 36, 158-171.
Gaw A, Packard CJ, Caslake MJ, Griffin BA, Lindsay GM, Thomson J, Vallance BD, Wosornu D & Shepherd J. (1994). Effects of ciprofibrate on LDL metabolism in man. Atherosclerosis 108, 137-148.
Watson TDG, Caslake MJ, Freeman D, Griffin BA, Hinnie C, Packard CJ & Shepherd J. (1994). Determinants of LDL subfraction distribution and concentrations in normolipidaemic subjects. Arteriosclerosis & Thrombosis 14, 902-910.
Griffin BA, Freeman DJ, Tait GW, Thomson J, Caslake MJ, Packard CJ & Shepherd J. (1994). Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions. Relative contribution of small, dense LDL to coronary heart disease risk. Atherosclerosis 106, 241-253.
Freeman DJ, Griffin BA, Holmes AP, Lindsay GM, Gaffney D, Packard CJ & Shepherd J. (1994). Regulation of plasma HDL cholesterol and subfraction distribution by genetic and environmental factors. Associations between the Taq I
B restriction length polymorphism in the CETP gene and smoking and obesity. Arteriosclerosis & Thrombosis 14, 336-344.
Freeman DJ, Griffin BA, Murray E, Lindsay GM, Gaffney D, Packard CJ & Shepherd J. (1993). Smoking and plasma lipoproteins: effects on cholesteryl ester transfer protein activity, low density lipoprotein cholesterol levels and high density lipoprotein subfraction distribution. European Journal of Clinical Investigation 23, 630-640.
Griffin BA, Farish E, Walsh D, Barnes J, Caslake MJ, Shepherd J & Hart D. (1993). Response of low density lipoprotein subfractions to oestrogen replacement therapy following surgical menopause. Clinical Endocrinology 39, 463-468.
Caslake MJ, Packard CJ, Gaw A, Murray EF, Griffin BA & Shepherd J. (1993). Fenofibrate and low density lipoprotein metabolic heterogeneity in hypercholesterolaemia. Arteriosclerosis & Thrombosis 13, 702-711.
Gaw A, Packard CJ, Murray EF, Linsay GM, Griffin BA, Caslake MJ, Vallance BD, Lorimer AR & Shepherd J. (1993). Effects of simvastatin on apolipoprotein metabolism and LDL subfraction distribution. Arteriosclerosis & Thrombosis 13, 170-189.
Wilson HM, Griffin BA, Watt C & Skinner ER. (1992). The isolation and characterisation of high density lipoprotein subfractions containing apolipoprotein E from human plasma. Biochemical Journal 284, 477-481.
Griffin BA, Caslake MJ, Gaw A, Sinnott M, Yip B, Packard CJ & Shepherd J. (1992). Effects of cholestyramine and acipimox on subfractions of plasma LDL. Studies in normal and hypercholesterolaemic subjects. European Journal of Clinical Investigation 22, 383-390.
Wojciechowski AP, Farrall PC, Wilson TME, Bayliss JD, Farren B, Griffin BA, Caslake MJ, Packard CJ, Shepherd J, Thakker R & Scott J. (1991). Familial combined hyper-lipoproteinaemia is linked to the apoprotein AI-CIII-AIV gene cluster on chromosome 11q23-q24. Nature 349, 161-164.
Griffin BA, Caslake MJ, Yip B, Tait GW, Packard CJ & Shepherd J. (1990). Rapid isolation of low density lipoprotein (LDL) subfractions from plasma by density gradient ultra-centrifugation. Atherosclerosis 83, 59-67.
Gaw A, Griffin BA, Caslake MJ, Collins SM, Lorimer AR, Packard CJ & Shepherd J. (1990). Effects of acipimox on apolipoprotein B metabolism and LDL subfraction distribution in hypercholesterolaemic subjects. Journal of Drug Development 3, 107-109.
Griffin BA, Skinner ER & Maughan RJ. (1988). The acute effects of prolonged walking and dietary changes on plasma lipoproteins and high-density lipoprotein subfractions. Metabolism 37, 535-541.
Griffin BA, Skinner ER & Maughan RJ. (1988). Plasma high-density lipoprotein subfractions in subjects with different coronary risk indices as assessed by lipoprotein concentrations. Atherosclerosis 70, 165-169.
Invited reviews, editorials and commentaries
Griffin BA & Lovegrove JA (2018) Butter increases HDL functional capacity: is this compensation for its adverse effect on serum LDL cholesterol? Journal of Nutrition (In press)
Griffin BA (2017) Serum low-density lipoprotein as a dietary responsive biomarker of cardiovascular disease risk: Consensus or confusion? British Nutrition Foundation. Nutrition Bulletin 42, 266-273.
Turner L, Poole K, Faithfull S & Griffin BA (2017) Current and future strategies for the nutritional management of cardio-metabolic complications of androgen deprivation therapy for prostate cancer Nutrition Research Reviews 13, 1-13.
Griffin BA (2015) Saturated fat: guidelines to reduce coronary heart disease risk are still valid. The Pharmaceutical Journal 294 (7858), Online URI 20068191.
Griffin BA (2014) Non-pharmacological approaches for reducing serum low-density lipoprotein cholesterol. Current Opinions in Cardiology 29, 360-365.
Gray J & Griffin BA (2013) Eggs: Establishing the nutritional benefits. British Nutrition Foundation. Nutrition Bulletin 38, 438-449.
Griffin BA (2013) Lipid metabolism. In: Surgery 31, 267-272.
Lovegrove JA & Griffin BA (2013). The acute and long-term effects of dietary fatty acids on vascular function in health and disease. Current Opinions in Nutrition & Metabolic Care 16, 162-167.
Griffin BA (2012) Goldilocks and the three bonds: new evidence for the conditional benefits of dietary alpha-linolenic acid in treating cardiovascular risk in the metabolic syndrome British Journal of Nutrition 108, 579-580,
Griffin BA, Agewall S (2012) Can increased arterial stiffness in women relative to men be explained by their progressive loss of gluteofemoral fat? Atherosclerosis 224, 320-321.
Lovegrove JA, Griffin BA (2011). Can dietary modification reduce the cardiovascular complications of metabolic syndrome? 'All for one' or 'one for all'? Expert Reviews in Cardiovascular Therapy 9, 413-416.
Mikhailidis DP, Elisaf MS, Rizzo M, Berneis K, Griffin B et al. (2011). "European Panel on Low Density Lipoprotein (LDL) Subclasses": A Statement on the Pathophysiology, Atherogenicity and Clinical Significance of LDL Subclasses: Executive Summary. Current Vascular Pharmacology 9, 531-532.
Mikhailidis DP, Elisaf MS, Rizzo M, Berneis K, Griffin B, et al. (2011). "European Panel on Low Density Lipoprotein (LDL) Subclasses": A Statement on the Pathophysiology, Atherogenicity and Clinical Significance of LDL Subclasses. Current Vascular Pharmacology 9, 533-571.
Griffin BA. (2011). Dairy, dairy, quite contrary: further evidence to support a role for calcium in counteracting the cholesterol-raising effect of SFA in dairy foods. British Journal of Nutrition 14, 1-2.
Griffin BA (2009) The nutritional properties of eggs. Journal of the Institute of Food and Technology 23, 14-16.
Gray J & Griffin B (2009). Eggs and dietary cholesterol - dispelling the myth. British Nutrition Foundation Nutrition Bulletin 34, 66-70.
Mason P, Porter SC, Berry SE, Stillman P, Steele C, Kirby A, Griffin BA & Minihane AM (2009). Saturated fatty acid consumption: outlining the scale of the problem and assessing the solutions. British Nutrition Foundation Nutrition Bulletin 34, 74-84.
Ferns G, Keti V & Griffin B (2008). Investigation and Management of Hyper- triglyceridaemia. Journal of Clinical Pathology 61:1174-1183.
Griffin BA (2008). Dietary cholesterol; not something for most people to worry about. The British Dietetic Association: Dietetics Today 44, 44-47.
Griffin BA (2008). How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP Study. Current Opinion in Lipidology 19: 57-62.
Jebb SA, Frost G, Griffin BA, Lovegrove JA, Moore C, Sanders T & Williams CM (2007). The RISCK Study; testing the impact of the amount and type of dietary fat and carbohydrate on metabolic risk. British Nutrition Foundation Bulletin 32, 154-156.
Stanley JC, Elsom RL, Calder PC, Griffin BA, Harris WS, Jebb JA, Lovegrove JA, Moore CS, Riemersma RA &.Sanders TAB (2007). The effects of the dietary n-6: n-3 fatty acid ratio on cardiovascular health: UK Food Standards Agency Workshop Report. British Journal of Nutrition 98, 1305-1310.
Lee A & Griffin BA (2006). Dietary cholesterol, eggs and coronary heart disease in perspective. British Nutrition Foundation Bulletin 31, 21-27.
Sanderson P, Olthof M, Grimble RF, Calder PC, Griffin BA, de Roos NM, Belch JJF, Muller DPR, & Vita JA (2004). Dietary lipids and vascular function: UK Food Standards Agency workshop report. British Journal of Nutrition 91, 491-500.
Mensink RP, Aro A, Hond ED, German B, Griffin BA, Meer HU, Mutanen M, Pannemans & Stahl W (2003). PASSCLAIM1 – Diet-related cardiovascular disease. European Journal of Nutrition 42 (Suppl. 1), 1/7-1/27.
Sanderson P, Finnegan YE, Williams CM, Calder PC, Burdge GC, Wooton SA, Griffin BA, Millward DJ, Pegge NC & Bemelmans WJE (2002). UK Food Standards Agency a-linolenic acid workshop report. British Journal of Nutrition 88, 573-579.
Griffin BA (2002) Omega-3 fatty acids in the treatment of diabetic dyslipidaemia. The Nutrition Practioner 4 (1), 35-37.
Griffin BA (2001). The effects of n-3 PUFA on LDL subfractions. Lipids 36, S91-S97.
Griffin BA (2001). Nutrition and Therapeutics (Editorial) Current Opinion in Lipidology 12, 457-459. (6.194)
Griffin BA & Fielding B (2001). Post-prandial lipid handling. Current Opinion in Clinical Nutrition and Metabolic Care 4, 93-98.
Griffin BA (2000). Nutrition and Metabolism (Editorial) Current Opinion in Lipidology 11, 425-427.
Griffin BA (1999). Cholesterol-lowering effects of high protein soya milk. British Journal of Nutrition 82, 79-80.
Griffin BA (1999). Small, dense atherogenic LDL - a silent risk factor. Cardiovascular Disease / Lipids Dialogue 9, 5-7.
Griffin BA (1998). Nutrition and Therapeutics (Editorial) Current Opinion in Lipidology 9, 267-269.
Griffin BA (1998). Small, dense low-density lipoprotein (LDL); A risk factor for coronary heart disease? Issues in Preventive Cardiology (edited by: Sniderman AD) 1, 10-14.
Griffin BA (1996). Nutrition and Therapeutics Current Opinion in Lipidology 7, U77-U88.
Griffin BA & Zampelas A. (1995). The influence of dietary fatty acids on the atherogenic lipoprotein phenotype. Nutrition Research Reviews (edited by: Gurr MI) 8,1-26.
Griffin BA (1995) Nutrition (Editorial). Current Opinions in Lipidology 6, U85-U89.
Griffin BA & Packard CJ (1994). Metabolism of VLDL and LDL subclasses. Current Opinions in Lipidology 5, 200-206.
Griffin BA. (1993). Lipid Metabolism (Editorial) Current Opinions in Lipidology 4, II-9 II-10.
Shepherd J, Griffin BA, Caslake MJ, Gaw A & Packard CJ. (1991). The influence of fibrates on lipoprotein metabolism. Atherosclerosis Reviews 22, 163-169.
Transactions and conference proceedings
Griffin BA (2016) Eggs: good or bad? Proceedings of the Nutrition Society 75, 259-264.
Griffin BA (2015) Relevance of liver fat to the impact of dietary extrinsic sugars on lipid metabolism. Proceedings of the Nutrition Society 74, 208-214.
Williams CM, Lovegrove JA, Griffin BA. (2013) Dietary patterns and cardiovascular disease. Proceedings of the Nutrition Society 72, 407-411.
Mitchell HL, Gibbins JM, Griffin BA, Lovegrove JA, Stowell JD, Foot E (2012) Food and Health Forum meeting:nutritional approaches to cardiovascular health: workshop report. British Nutrition Foundation Nutrition Bulletin (Epub ahead of print)
Cassidy A & Griffin BA (1999). Oestrogens and lipid-mediated CHD risk. Proceedings of the Nutrition Society 58, 193-199.
Griffin BA (1999). Lipoprotein atherogenicity: an overview of current mechanisms. Proceedings of the Nutrition Society 58, 163-169.
Griffin BA. (1997). Low-density lipoprotein subclasses: mechanisms of formation and modulation. Proceedings of the Nutrition Society 56, 1-10.
Gaw A, Griffin BA, Gaffney D, Caslake MJ, Packard CJ & Shepherd J. (1990). Genetic and environmental modulation of low density lipoprotein catabolism. Biochemical Society Transactions 18, 1072-1074.
Packard CJ, Caslake MJ, Griffin BA, Gaw A, Shepherd J. (1990). Fenofibrate and lipoprotein metabolism. Drugs in Focus. Summary Proceedings of the 3rd International Workshop on Lipid Metabolism, Dijon, France pp 9-10.
Griffin BA, Skinner ER & Maughan RJ. (1986). Changes in plasma LCAT activity during aerobic exercise. Biochemical Society Transactions 14, 1094-1095.
Griffin BA (2018) 30 Seconds of Nutrition - ‘Fats’, ‘Metabolism’, ‘Eggs’, ‘Dietary Fats & Cardiovascular Disease’ ‘Profile on Ancel Keys’ (Edited by Lovegrove JA) Published by Ivy Press (In press).
Escolà-Gil JC, Julve J, Griffin BA, Freeman D, Blanco-Vaca F (2015) HDL and lifestyle interventions. Handbook of Experimental Pharmacology 224, 569-92.
Griffin BA (2011). Eggs, dietary cholesterol and disease: facts and folklore. In: Improving the safety and quality of eggs and egg products Vol. 2 Egg Safety and nutritional quality Eds: Immerseel FV, Nys Y and Bain M Published by Woodhead Publishing Ltd. ISBN 978-85709-072-0
Griffin BA (2008). Nutrition and metabolism of lipids. In: Introduction to Human Nutrition. 2nd Edition. Published by Blackwell Sciences Ltd
Whitehead K & Griffin BA (2003). Lifestyle management: Diet. In: Coronary heart disease prevention: a handbook for the health care team. Second Edition (Edited by Lindsay GM & Gaw A) Churchill Livingstone, pp:107-137.
Griffin BA, Wright JW. (1998). Assessment of cholesterol status: identification of small, dense LDL. In: Methodological Surveys in Bio-analysis of Drugs 25, (edited by: Reid E, Hill HM & Wilson ID) Published by the Royal Society of Chemistry. pp: 258-262 ISBN: 0-85404-748-4.
Cunnane SC & Griffin BA (2002). Nutrition and metabolism of lipids. In: Introduction to Human Nutrition. Eds. Gibney MJ, Vorster HH & Kok FJ. pp: 81-115 Blackwell Sciences Ltd.
Graham JM, Griffin BA, Davies IG & Higgins JA. (2000). Fractionation of lipoprotein subclasses in self-generated gradients of iodixanol. Atherosclerosis: methods and protocols, In: Methods in Molecular Biology (edited by: Drew AF) Humana Press pp: 51-61.
Griffin BA (2001). Current evidence for effects of dietary cholesterol. In: Dietary cholesterol as a cardiac risk factor: myth or reality. (edited by: Leeds AR & Gray J). Published by Smith-Gordon & Co Ltd, pp: 27-34.
Gilbert NG & Griffin BA. (1997). Lifestyle management: Diet. In: Coronary Heart Disease Prevention: A Handbook for the Healthcare Team. (edited by: Gaw A & Lindsay GM) Churchill & Livingstone 6, pp: 107-138. ISBN 0-443-05460-6.
Griffin BA. (1995). Low density lipoprotein heterogeneity. In: Bailliere’s Clinical Endocrinology & Metabolism (edited by: Betteridge DJ) 9 (4), 687-703.ISBN: 0-702-01982-8.
Objective SNPs identified from genome-wide association studies associate with lipid risk markers of cardiovascular disease. This study investigated whether these SNPs altered the plasma lipid response to diet in the ‘RISCK’ study cohort. Methods Participants (n = 490) from a dietary intervention to lower saturated fat by replacement with carbohydrate or monounsaturated fat, were genotyped for 39 lipid-associated SNPs. The association of each individual SNP, and of the SNPs combined (using genetic predisposition scores), with plasma lipid concentrations was assessed at baseline, and on change in response to 24 weeks on diets. Results The associations between SNPs and lipid concentrations were directionally consistent with previous findings. The genetic predisposition scores were associated with higher baseline concentrations of plasma total (P = 0.02) and LDL (P = 0.002) cholesterol, triglycerides (P = 0.001) and apolipoprotein B (P = 0.004), and with lower baseline concentrations of HDL cholesterol (P < 0.001) and apolipoprotein A-I (P < 0.001). None of the SNPs showed significant association with the reduction of plasma lipids in response to the dietary interventions and there was no evidence of diet-gene interactions. Conclusion Results from this exploratory study have shown that increased genetic predisposition was associated with an unfavourable plasma lipid profile at baseline, but did not influence the improvement in lipid profiles by the low-saturated-fat diets.
Objective: The PPARG SNP rs1801282 (Pro12Ala C>G) has shown variable association with metabolic syndrome traits in healthy subjects. We investigated genotype association with plasma lipids and the influence of dietary polyunsaturated:saturated fat ratio (P:S) in subjects at increased cardiometabolic risk. Methods: Habitual dietary intake was recorded at recruitment to the RISCK Study. PPARG rs1801282 was genotyped in 466 subjects aged 30-70 y. Genotype associations with plasma lipids were assessed at recruitment, after a 4-wk high-SFA (HS) diet and a 24-wk intervention with reference (HS), high-MUFA (HM) and low-fat (LF) diets. The interaction of habitual P:S intake x genotype on plasma lipid concentrations was investigated. Results: PPARG rs1801282 G-allele frequency was 0.09. At recruitment, G-allele carriers had higher plasma total cholesterol concentration (n=415; P=0.05) after adjustment for BMI, gender, age and ethnicity. Dietary P:S ratio x genotype interaction influenced plasma LDLcholesterol (P=0.02) and triglyceride (P=0.03) concentrations. At P:S ratio 0.33, mean LDLcholesterol concentration in G-allele carriers was higher than in non-carriers, but fell between 0.34-0.65. Triglyceride concentration followed a similar pattern. After the 4-wk HS diet, Gallele carriers had higher concentrations of total cholesterol (P=0.03), LDL-cholesterol (P=0.04) and apo B (P=0.04) than non-carriers, after adjustments. After the 24-wk interventions, diet x genotype interaction did not significantly influence either LDLcholesterol (P=0.58) or triglyceride (P=0.57) concentrations. Conclusion: A high dietary P:S ratio would help to reduce plasma LDL-cholesterol and triglyceride concentrations in PPARG rs1801282 G-allele carriers at increased cardiometabolic risk.
Background: When advising patients on diet and health, the general practitioner (GP) makes judgements based on the evidence available. Since current evidence on diet and cardiovascular disease is conflicted and confusing, we surveyed the current consensus amongst GPs. The aim of this study was to determine the views of GPs on dietary saturated fat, carbohydrates and long chain omega-3 fatty acids in the management of cardiovascular disease. Method: An online questionnaire inviting participants to comment on seven contentious statements on diet and cardiovascular disease. Questionnaire circulated to the 1800 members of South West Thames Faculty of the Royal College of General Practitioners (RCGP). Participants were invited to tick “ Agree ” , “ Disagree ” or “ Not sure ” and were encouraged to add comments for each question. The results were analysed with a combination of statistical analysis and thematic analysis of comments. Results: There were 89 responses. Most GPs seem well aware that drug treatment alone is inadequate and that dietary advice is important. However, there was con siderable disagreement about the roles of saturated fats and carbohydrates in ca rdiovascular disease and “ Not sure ” responses ranged from 12 to 40.7%. The 40. 7% related to a statement on long chain omega-3 fatty acids. Analysis of comments revealed more opinions including an awareness of the need to warn patients about trans -fatty acids. Conclusions: Although the GP response rate was poor, responders do seem to see dietary advice as part of their role but do not consider themselves as experts. Education in this area should have a higher priority.
BACKGROUND: Dietary alpha-linolenic acid (ALA) has been associated with reduced risk of development of atherosclerosis. Adiponectin is a hormone specifically secreted by adipocytes and considered to have anti-atherogenic properties. AIM OF THE STUDY: We examined the effect of increased dietary intake of ALA on plasma concentration of adiponectin. METHODS: Thirty-five non-diabetic, dyslipidemic men, 38-71 years old, were randomly allocated to take either 15 ml of flaxseed oil rich in ALA (8.1 g/day; n = 18), or 15 ml of safflower oil per day, containing the equivalent n-6 fatty acid (11.2 g/day linoleic acid, LA; n = 17) (control group). The intervention period lasted for 12 weeks. RESULTS: Plasma levels of adiponectin did not change after the increase in dietary intake of ALA in the flaxseed oil supplementation group, compared to the control group. No changes in body mass index, serum lipid concentrations, LDL density, or plasma TNF-alpha were found in the flaxseed oil versus the control group. CONCLUSIONS: Dietary ALA has no effect on plasma adiponectin concentration in dyslipidemic men.
PURPOSE OF REVIEW: Vascular function is recognized as an early and integrative marker of cardiovascular disease. While there is consistent evidence that the quantity of dietary fat has significant effects on vascular function, the differential effects of individual fatty acids is less clear. This review summarizes recent evidence from randomly controlled dietary studies on the impact of dietary fatty acids on vascular function, as determined by flow-mediated dilatation (FMD). RECENT FINDINGS: Critical appraisal is given to five intervention studies (one acute, four chronic) which examined the impact of long-chain n-3 polyunsaturated fatty acid [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] on FMD. In the acute setting, a high dose of long-chain n-3 polyunsaturated fatty acid (4.9 g per 70 kg man) improved postprandial FMD significantly, compared with a saturated fatty acid-rich meal in healthy individuals. In longer-term studies, there was limited evidence for a significant effect of EPA/DHA on FMD in diseased groups. SUMMARY: The strongest evidence for the benefits of EPA/DHA on vascular function is in the postprandial state. More evidence from randomly controlled intervention trials with foods will be required to substantiate the long-term effects of EPA/DHA, to inform public health and clinical recommendations.
Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD) and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on plasma lipoproteins. To study this further, men with NAFLD (n=11) and low liver fat ‘controls’ (n= 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and lipoprotein kinetics were measured after each diet by stable isotope trace-labelling. There were significant differences in the production and catabolic rates of VLDL subclasses between men with NAFLD and controls, in response to the high and low sugar diets. Men with NAFLD had higher plasma concentrations of VLDL1-triacylglycerol (TAG) after the high (P
Context:Maternal obesity is associated with high plasma triglyceride, poor vascular function, and an increased risk for pregnancy complications. In normal-weight pregnant women, higher triglyceride is associated with increased small, dense low-density lipoprotein (LDL).Hypothesis:In obese pregnancy, increased plasma triglyceride concentrations result in triglyceride enrichment of very low-density lipoprotein-1 particles and formation of small dense LDL via lipoprotein lipase.Design:Women (n = 55) of body mass index of 18-46 kg/m(2) were sampled longitudinally at 12, 26, and 35 weeks' gestation and 4 months postnatally.Setting:Women were recruited at hospital antenatal appointments, and study visits were in a clinical research suite.Outcome Measures:Plasma concentrations of lipids, triglyceride-rich lipoproteins, lipoprotein lipase mass, estradiol, steroid hormone binding globulin, insulin, glucose, leptin, and adiponectin were determined.Results:Obese women commenced pregnancy with higher plasma triglyceride, reached the same maximum, and then returned to higher postnatal levels than normal-weight women. Estradiol response to pregnancy (trimester 1-3 incremental area under the curve) was positively associated with plasma triglyceride response (r(2) adjusted 25%, P < .001). In the third trimester, the proportion of small, dense LDL was 2-fold higher in obese women than normal-weight women [mean (SD) 40.7 (18.8) vs 21.9 (10.9)%, P = .014], and 35% of obese, 14% of overweight, and none of the normal-weight women displayed an atherogenic LDL subfraction phenotype. The small, dense LDL mass response to pregnancy was inversely associated with adiponectin response (17%, P = .013).Conclusions:Maternal obesity is associated with an atherogenic LDL subfraction phenotype and may provide a mechanistic link to poor vascular function and adverse pregnancy outcome.
Androgen deprivation therapy (ADT) is used widely as part of a combined modality for the treatment of prostate cancer. However, ADT has also been associated with the development of cardiometabolic complications that can increase mortality from cardiovascular events. There is emerging evidence to suggest that ADT-related cardiometabolic risk can be mitigated by diet and lifestyle modification. While the clinical focus for a nutritional approach for achieving this effect is unclear, it may depend upon the timely assessment and targeting of dietary changes to the specific risk phenotype of the patient. The present review aims to address the metabolic origins of ADT-related cardiometabolic risk, existing evidence for the effects of dietary intervention in modifying this risk, and the priorities for future dietary strategies.
The replacement of saturated fatty acids (SFA) has been the mainstay of our dietary guidelines to help prevent cardiovascular disease (CVD) for over 30 years. However, the underlying evidence to support this guideline is now held in contentious disrepute on the grounds of an apparent lack of evidence, largely from meta-analyses, for a direct relationship between saturated fat and CVD mortality. This can be explained by the fact that the relationship between dietary SFA and CVD is not direct, but indirect and mediated through the low-density lipoprotein cholesterol (LDL-C) raising effects of certain SFA, in certain foods. There is over 100 years of evidence to link raised serum cholesterol with CVD and to support the current consensus that serum LDL is causally related to CVD morbidity and mortality. Nevertheless, the role of LDL as a biomarker of CVD risk, as measured by its cholesterol content (LDL-C), is often confused with its contribution to cardio-metabolic risk by its conversion into small and dense LDL particles with increased potential to cause CVD. The clinical utility of serum LDL is outstanding as a biomarker for CVD, albeit through an increase in its cholesterol mass (LDL-C), its small particle size or over-abundance of these particles. What is of overriding importance is to identify and modify these characteristics in LDL at the earliest stage of their development and to reduce the associated CVD risk through appropriate and sustained changes in diet and lifestyle.
Findings from epidemiological studies over the past 30 years have shown that visceral adipose tissue, accurately measured by CT or MRI, is an independent risk marker of cardiovascular and metabolic morbidity and mortality. Emerging evidence also suggests that ectopic fat deposition, including hepatic and epicardial fat, might contribute to increased atherosclerosis and cardiometabolic risk. This joint position statement from the International Atherosclerosis Society and the International Chair on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral adiposity and ectopic fat as emerging risk factors for type 2 diabetes, atherosclerosis, and cardiovascular disease, with a focus on practical recommendations for health professionals and future directions for research and clinical practice. We discuss the measurement of visceral and ectopic fat, pathophysiology and contribution to adverse health outcomes, response to treatment, and lessons from a public health programme targeting visceral and ectopic fat. We identify knowledge gaps and note the need to develop simple, clinically applicable tools to be able to monitor changes in visceral and ectopic fat over time. Finally, we recognise the need for public health messaging to focus on visceral and ectopic fat in addition to excess bodyweight to better combat the growing epidemic of obesity worldwide.
Nightshift work is associated with adverse health outcomes, which may be related to eating during the biological night, when circadian rhythms and food intake are misaligned. Nurses often undertake nightshift work, and we aimed to investigate patterns of energy distribution and dietary intake across 14 days in 20 UK National Health Service (NHS) nurses working rotational shifts. We hypothesised that the proportion of daily energy consumed during the nightshift would increase over consecutive nights. Primary and secondary outcome measures included intakes of energy and macronutrients. Our results show that nurses consumed the same total daily energy on nightshifts and non-nightshifts, but redistributed energy to the nightshift period in increasing proportions with a significant difference between Night 1 and 2 in the proportion of total daily energy consumed (26.0 ± 15.7% vs. 33.5 ± 20.2%, mean ± SD; p < 0.01). This finding indicates that, rather than increasing total energy intake, nurses redistribute energy consumed during nightshifts as a behavioural response to consecutive nightshifts. This finding informs our understanding of how the intake of energy during the biological night can influence adverse health outcomes of nightshift work.
Background Assessing fitness and promoting regular physical activity can improve health outcomes and early recovery in prostate cancer. This is however, underutilised in clinical practice. The cardiopulmonary exercise test (CPET) is increasingly being used pre-treatment to measure aerobic capacity and peak oxygen consumption (VO2peak - a gold standard in cardiopulmonary fitness assessment). However, CPET requires expensive equipment and may not always be appropriate. The Siconolfi step test (SST) is simpler and cheaper, and could provide an alternative. The aim of this study was to evaluate the validity and reliability of SST for predicting cardiopulmonary fitness in men with prostate cancer. Men were recruited to this two-centre study (Surrey and Newcastle, United Kingdom) after treatment for locally advanced prostate cancer. They had one or more of three risk factors: elevated blood pressure, overweight (BMI ˃ 25), or androgen deprivation therapy (ADT). Cardiopulmonary fitness was measured using SST and cycle ergometry CPET, at two visits three months apart. The validity of SST was assessed by comparing it to CPET. The VO2peak predicted from SST was compared to the VO2peak directly measured with CPET. The reliability of SST was assessed by comparing repeated measures. Bland-Altman analysis was used to derive limits of agreement in validity and reliability analysis. Results Sixty-six men provided data for both SST and CPET. These data were used for validity analysis. 56 men provided SST data on both visits. These data were used for reliability analysis. SST provided valid prediction of the cardiopulmonary fitness in men ˃ 60 years old. The average difference between CPET and SST was 0.64 ml/kg/min with non-significant positive bias towards CPET (P = 0.217). Bland-Altman 95% limits of agreement of SST with CPET were ± 7.62 ml/kg/min. SST was reliable across the whole age range. Predicted VO2peak was on average 0.53 ml/kg/min higher at Visit 2 than at Visit 1 (P = 0.181). Bland-Altman 95% limits of agreement between repeated SST measures were ± 5.84 ml/kg/min. Conclusions SST provides a valid and reliable alternative to CPET for the assessment of cardiopulmonary fitness in older men with prostate cancer. Caution is advised when assessing men 60 years old or younger because the VO2peak predicted with SST was significantly lower than that measured with CPET.
Despite decades of unequivocal evidence that waist circumference provides both independent and additive information to BMI for predicting morbidity and risk of death, this measurement is not routinely obtained in clinical practice. This Consensus Statement proposes that measurements of waist circumference afford practitioners with an important opportunity to improve the management and health of patients. We argue that BMI alone is not sufficient to properly assess or manage the cardiometabolic risk associated with increased adiposity in adults and provide a thorough review of the evidence that will empower health practitioners and professional societies to routinely include waist circumference in the evaluation and management of patients with overweight or obesity. We recommend that decreases in waist circumference are a critically important treatment target for reducing adverse health risks for both men and women. Moreover, we describe evidence that clinically relevant reductions in waist circumference can be achieved by routine, moderate-intensity exercise and/or dietary interventions. We identify gaps in the knowledge, including the refinement of waist circumference threshold values for a given BMI category, to optimize obesity risk stratification across age, sex and ethnicity. We recommend that health professionals are trained to properly perform this simple measurement and consider it as an important 'vital sign' in clinical practice.
Context: Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. Objective: To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. Design Longitudinal study throughout gestation and at delivery. Setting Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. Patients Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. Methods: Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. Main Outcome Measures Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin. Results: VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). Conclusions: Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport.
Objective: To determine the effect of prolonged exposure to a submarine environment on biomarkers of cardiometabolic risk in Royal Navy (RN) submariners.
A Nutrition Society member-led meeting was held on 9 January 2020 at The University of Surrey, UK. Sixty people registered for the event, and all were invited to participate, either through chairing a session, presenting a ‘3 min lightning talk’ or by presenting a poster. The meeting consisted of an introduction to the topic by Dr Barbara Fielding, with presentations from eight invited speakers. There were also eight lightning talks and a poster session. The meeting aimed to highlight recent research that has used stable isotope tracer techniques to understand human metabolism. Such studies have irrefutably shaped our current understanding of metabolism and yet remain a mystery to many. The meeting aimed to de-mystify their use in nutrition research.
The purpose of this study was to compare fitness parameters and cardiovascular disease risk of older and younger men with prostate cancer (PCa) and explore how men's fitness scores compared to normative age values. 83 men were recruited post-treatment and undertook a cardiopulmonary exercise test (CPET), sit-to-stand, step-and-grip strength tests and provided blood samples for serum lipids and HbA1c. We calculated waist-to-hip ratio, cardiovascular risk (QRISK2), Charlson comorbidity index (CCI) and Godin leisure-time exercise questionnaire [GLTEQ]. Age-group comparisons were made using normative data. Men > 75 years, had lower cardiopulmonary fitness, as measured by VO2 Peak (ml/kg/min) 15.8 + 3.8 p < 0.001, and lower grip strength(28.6+5.2 kg p < 0.001) than younger men. BMI ≥30kg/m2 and higher blood pressure all contributed to a QRisk2 score indicative of 20% chance of cardiovascular risk within 10 years (mean: 36.9–6.1) p < 0.001. Age, BMI and perceived physical activity were significantly associated with lower cardiopulmonary fitness. Men with PCa > 75 years had more cardiovascular risk factors compared to normative standards for men of their age. Although ADT was more frequent in older men, this was not found to be associated with cardiopulmonary fitness, but obesity and low levels of physical activity were. Secondary prevention should be addressed in men with PCa to improve men's overall health.
In this Second Edition of the introductory text in the acclaimed Nutrition Society Textbook Series, "Introduction to Human Nutrition" has been revised and ...
Objective It is well established that exercise and lifestyle behaviours improve men's health outcomes from prostate cancer. With 3.8 million men living with the disease worldwide, the challenge is creating accessible intervention approaches that lead to sustainable lifestyle changes. We carried out a phase II feasibility study of a lifestyle intervention delivered by nine community pharmacies in the United Kingdom to inform a larger efficacy study. Qualitative interviews explored how men experienced the intervention, and these data are presented here. Methods Community pharmacies delivered a multicomponent lifestyle intervention to 116 men with prostate cancer. The intervention included a health, strength, and fitness assessment, immediate feedback, lifestyle prescription with telephone support, and reassessment 12 weeks later. Three months after receiving the intervention, 33 participants took part in semistructured telephone interviews. Results Our framework analysis identified how a teachable moment can be created by a community pharmacy intervention. There was evidence of this when men's self‐perception was challenged and coupled to a positive interaction with a pharmacist. Our findings highlight the social context of behaviour change with men identifying how their lifestyle choices were negotiated within their household. There was a ripple effect as lifestyle behaviours made a positive impact on friends and family. Conclusions The teachable moment is not a serendipitous opportunity but can be created by an intervention. Our study adds insight into how community pharmacists can support cancer survivors to make positive lifestyle behaviour changes and suggests a role for doing rather than just telling.
Background & Aims: Serum lipids and lipoproteins are established biomarkers of cardiovascular disease risk that could be influenced by impaired gut barrier function via effects on the absorption of dietary and biliary cholesterol. The aim of this study was to examine the potential relationship between gut barrier function (gut permeability) and concentration of serum lipids and lipoproteins, in an ancillary analysis of serum samples taken from a previous study. Methods and Results: Serum lipids, lipoproteins and functional gut permeability, as assessed by the percentage of the urinary recovery of 51-Cr-labelled EDTA absorbed within 24h, were measured in a group of 30 healthy men. Serum lipopolysaccharide, high sensitivity C-reactive protein and interleukin-6 were also measured as markers of low-grade inflammation. The group expressed a 5- fold variation in total gut permeability (1.11 - 5.03%). Gut permeability was unrelated to the concentration of both serum total and low density lipoprotein (LDL)-cholesterol, but was positively associated with serum high density lipoprotein (HDL)-cholesterol (r=0.434, P=0.015). Serum HDL cholesterol was also positively associated with serum endotoxaemia (r=0.415, p=0.023). Conclusion: The significant association between increased gut permeability and elevated serum HDL-cholesterol is consistent with the role of HDL as an acute phase reactant, and in this situation, potentially dysfunctional lipoprotein. This finding may have negative implications for the putative role of HDL as a cardio-protective lipoprotein.
A cross-sectional analysis of ethnic differences in dietary intake, insulin sensitivity and beta-cell function, using the intravenous glucose tolerance test (IVGTT), was conducted on 497 healthy adult participants of the 'Reading, Imperial, Surrey, Cambridge, and Kings' (RISCK) study. Insulin sensitivity (Si) was significantly lower in African-Caribbean (AC) and South Asian (SA) participants [IVGTT-Si; AC: 2.13 vs SA: 2.25 vs white-European (WE): 2.84 (×10(-4) mL µU min)(2), p < 0.001]. AC participants had a higher prevalence of anti-hypertensive therapy (AC: 19.7% vs SA: 7.5%), the most cardioprotective lipid profile [total:high-density lipoprotein (HDL); AC: 3.52 vs SA: 4.08 vs WE: 3.83, p = 0.03] and more pronounced hyperinsulinaemia [IVGTT-acute insulin response (AIR)] [AC: 575 vs SA: 428 vs WE: 344 mL/µU/min)(2), p = 0.002], specifically in female participants. Intake of saturated fat and carbohydrate was lower and higher in AC (10.9% and 50.4%) and SA (11.1% and 52.3%), respectively, compared to WE (13.6% and 43.8%, p < 0.001). Insulin resistance in ACs is characterised by 'normal' lipid profiles but high rates of hypertension and pronounced hyperinsulinaemia.
The link between dietary fat and coronary heart disease has attracted much attention since the effect of long-chain fatty acids on gene transcription has been established. The aim of this study was to investigate the effects of long-chain fatty acids and clofibrate on mRNA levels of specific lipid metabolism-related genes and to determine their effects on global transcriptome levels in a cardiovascular cell-line.
The Oxford English Dictionary defines the word myth as; 'a popular idea concerning natural or historical phenomena ... that has no foundation in fact'. The popular idea in this context is that eating dietary cholesterol, typically from eggs, increases the risk of developing coronary heart disease (CHD), because it increases blood cholesterol. This contentious idea prevails, despite a lack of scientific foundation to support its existence, and almost global re-vamping of dietary recommendations to lift restrictions on the intake of cholesterol-rich foods. In an attempt to dispel the mythical status of dietary cholesterol and CHD, the following chapter will examine the role of dietary cholesterol in relation to what has been well established in terms of the relationships between blood cholesterol, diet and CHD. © 2011 Woodhead Publishing Limited All rights reserved.
The main lifestyle interventions to modify serum HDL cholesterol include physical exercise, weight loss with either caloric restriction or specific dietary approaches, and smoking cessation. Moderate alcohol consumption can be permitted in some cases. However, as these interventions exert multiple effects, it is often difficult to discern which is responsible for improvement in HDL outcomes. It is particularly noteworthy that recent data questions the use of HDL cholesterol as a risk factor and therapeutic target since randomised interventions and Mendelian randomisation studies failed to provide evidence for such an approach. Therefore, these current data should be considered when reading and interpreting this review. Further studies are needed to document the effect of lifestyle changes on HDL structure-function and health.
Despite decades of unequivocal evidence that waist circumference provides both independent and additive information to BMI for predicting morbidity and risk of death, this measurement is not routinely obtained in clinical practice. This Consensus Statement proposes that measurements of waist circumference afford practitioners with an important opportunity to improve the management and health of patients. We argue that BMI alone is not sufficient to properly assess or manage the cardiometabolic risk associated with increased adiposity in adults and provide a thorough review of the evidence that will empower health practitioners and professional societies to routinely include waist circumference in the evaluation and management of patients with overweight or obesity. We recommend that decreases in waist circumference are a critically important treatment target for reducing adverse health risks for both men and women. Moreover, we describe evidence that clinically relevant reductions in waist circumference can be achieved by routine, moderate- intensity exercise and/or dietary interventions. We identify gaps in the knowledge, including the refinement of waist circumference threshold values for a given BMI category , to optimize obesity risk stratification across age, sex and ethnicity. We recommend that health professionals are trained to properly perform this simple measurement and consider it as an important ‘vital sign’ in clinical practice.
The idea that dietary cholesterol increases risk of coronary heart disease (CHD) by turning into blood cholesterol is compelling in much the same way that fish oil improves arthritis by lubricating our joints! Dietary cholesterol, chiefly in the form of eggs, has long been outlawed as a causative agent in CHD through its association with serum cholesterol. However, the scientific evidence to support a role for dietary cholesterol in CHD is relatively insubstantial in comparison with the incontrovertible link between its circulating blood relative in low density lipoprotein (LDL) cholesterol and CHD. Interpretation of the relationship between dietary cholesterol and CHD has been repeatedly confounded by an often inseparable relationship between dietary cholesterol and saturated fat. It has also been exaggerated by the feeding of unphysiologically high intakes of eggs. Nonetheless, numerous studies have shown that dietary cholesterol can increase serum LDL-cholesterol, but the size of this effect is highly variable between individuals and, according to over 30 years of prospective epidemiology, has no clinically significant impact on CHD risk. Variation in response to dietary cholesterol is a real phenomenon and we can now identify nutrient-gene interactions that give rise to this variation through differences in cholesterol homeostasis. More importantly, to view eggs solely in terms of the effects of their dietary cholesterol on serum cholesterol is to ignore the potential benefits of egg consumption on coronary risk factors, including obesity, diabetes and metabolic syndrome. Cardiovascular risk in these conditions is largely independent of LDL-cholesterol. These conditions are also relatively unresponsive to any LDL-cholesterol raising effects of dietary cholesterol. Treatment is focused primarily on weight loss, and it is in this respect that eggs may have a new and emerging role in facilitating weight loss through increased satiety. © 2006 British Nutrition Foundation.
We examined the impact of APOE genotype on plasma lipids and glucose in a secondary analysis of data from a five-arm, randomised controlled, parallel dietary intervention trial (‘RISCK’ study), to investigate the impact of replacing saturated fatty acids (SFA) with either monounsaturated fat (MUFA) or carbohydrate of high or low glycaemic index (GI) on CVD risk factors and insulin sensitivity. We tested the impact of APOE genotype (carriage of E2 and E4 alleles versus E3/E3), determined retrospectively, on plasma lipids, lipoproteins and glucose homeostasis at baseline (n = 469), and on the change in these variables after 24 weeks of dietary intervention (n = 389). At baseline, carriers of E2 (n = 70), E4 (n = 125) and E3/E3 (n = 274) expressed marked differences in total plasma cholesterol (TC, p = 0.001), low density lipoprotein cholesterol (LDL-C, p < 0.0001), apolipoprotein B (apo B, p < 0.0001) and total to high density lipoprotein cholesterol ratio (TC:HDL-C, p = 0.002), with plasma concentrations decreasing in the order E4 > E3/E3 > E2. Following intervention, there was evidence of a significant diet x genotype interaction with significantly greater decreases in TC (p = 0.02) and apo B (p = 0.006) among carriers of E4 when SFA was replaced with low GI carbohydrate on a lower fat diet (TC −0.28 mmol/L p = 0.03; apo B −0.1 g/L p = 0.02), and a relative increase in TC (in comparison to E3/E3) when SFA was replaced with MUFA and high GI carbohydrates (TC 0.3 mmol/L, p = 0.03). Among carriers of E2 (compared with E3/E3) there was an increase in triacylglycerol (TAG) when SFA was replaced with MUFA and low GI carbohydrates 0.46 mmol/L p = 0.001). There were no significant interactions between APOE genotype and diet for changes in indices of glucose homeostasis. In conclusion, variations in APOE genotype led to differential effects on the lipid response to the replacement of SFA with MUFA and low GI carbohydrates.
Objectives: To assess the feasibility and acceptability of a community pharmacy lifestyle intervention to improve physical activity and cardiovascular health of men with prostate cancer. To refine the intervention. Design: Phase II feasibility study of a complex intervention. Setting: Nine community pharmacies in the UK. Intervention: Community pharmacy teams were trained to deliver a health assessment including fitness, strength and anthropometric measures. A computer algorithm generated a personalised lifestyle prescription for a homebased programme accompanied by supporting resources. The health assessment was repeated 12 weeks later and support phone calls were provided at weeks 1 and 6. Participants: 116 men who completed treatment for prostate cancer. Outcome measures: The feasibility and acceptability of the intervention and the delivery model were assessed by evaluating study processes (rate of participant recruitment, consent, retention and adverse events), by analysing delivery data and semi-structured interviews with participants and by focus groups with pharmacy teams. Physical activity (measured with accelerometry at baseline, 3 and 6 months) and patient reported outcomes (activation, dietary intake and quality of life) were evaluated. Change in physical activity was used to inform the sample size calculations for a future trial. Results: Out of 403 invited men, 172 (43%) responded and 116 (29%) participated. Of these, 99 (85%) completed the intervention and 88 (76%) completed the 6-month follow-up (attrition 24%). Certain components of the intervention were feasible and acceptable (eg, community pharmacy delivery), while others were more challenging (eg, fitness assessment) and will be refined for future studies. By 3 months, moderate to vigorous physical activity increased on average by 34 min (95% CI 6 to 62, p=0.018), but this was not sustained over 6 months. Conclusions: The community pharmacy intervention was feasible and acceptable. Results are encouraging and warrant a definitive trial to assess the effectiveness of the refined intervention.
Re-examination of the evidence for the relationship between dietary cholesterol in eggs, blood cholesterol and heart disease has clarified that the effects of the dietary cholesterol on LDL do not translate into increased risk of developing coronary heart disease for the majority of the population. The resultant lifting of the restriction on the consumption of eggs should help to persuade healthy but limited egg-eaters to put aside their misconceptions and increase general access to the nutritional benefits of eggs. Unfortunately, food policy is not always driven by the weight of scientific evidence, but by the cost-effectiveness of a practice or behaviour. To this end, a recent study performed an analysis of the economic impact of eggs in terms of the risks and benefits of eating eggs as compared to the costs of developing disease from not eating eggs (17). The conclusion was that limiting egg consumption was not cost effective from a societal perspective and that removing the nutritional benefits of eggs could lead to other, less affordable, disease outcomes. Let's hope that we are all right.
While the precise definition of hypertriglyceridaemia remains contentious, the condition is becoming more common in western populations as the prevalence of obesity and diabetes mellitus rise. Although there is strong epidemiological evidence that hypertriglyceridaemia is an independent risk factor for cardiovascular disease, it is has been difficult to demonstrate this by drug intervention studies, as drugs that reduce triglycerides also raise high density lipoprotein cholesterol. Precise target values have also been difficult to agree, although several of the new guidelines for coronary risk management now include triglycerides. The causes of hypertriglyceridaemia are numerous. The more severe forms have a genetic basis, and may lead to an increased risk of pancreatitis. Several types of hypertriglyceridaemia are familial and are associated with increased cardiovascular risk. Secondary causes of hypertriglyceridaemia are also numerous and it is important to exclude these before starting treatment with specific triglyceride-lowering agents. Lifestyle management is also very effective and includes weight reduction, restricted alcohol and fat intake and exercise.