This is a substantial number of people with maladaptive functioning. Taken together, the FA perspective suggests that biochemical changes and genetic predisposition to addiction can lead to excess food consumption independent of social factors. An important theme that has emerged is that FA is both an individual problem as well as a collective problem that should be addressed on a societal level.
Given the obesity trends and more recently the opioid epidemic, it can be argued that addiction is the number one public health problem in the United States. Research into the interaction between food addiction and eating disorders EDs , specifically binge eating disorder BED and bulimia nervosa BN , has led to conclusions of separate but related constructs. It has been proposed that those who meet criteria for BN should be separated into distinct subtypes: hyporesponsive to reward akin to anorexia nervosa and those with hypersensitive reward circuitry akin to FA The biggest gap in our understanding of the interaction between FA and EDs is the restrictive eating component.
There are many detractors of the FA hypothesis from the ED treatment community who argue that dieting also referred to as restrained eating is what causes elevated scores on the YFAS. It has also been argued that the role played by ingested substances is nonspecific meaning that they apply to EDs as well Future research should control for restrained eating, which has not been adequately done.
So, it is not surprising that high prevalence of FA occurs in the underweight category , and normal weight category in the case of BN Recently investigators have suggested that FA data can be incorporated into the case conceptualization of EDs from a trans-diagnostic perspective , Conclusions suggest giving more consideration to the impact of highly palatable foods for some people seeking ED treatment.
A few studies have linked FA and SUD , but additional research should be conducted on individuals with SUD in order to further understand how eating behaviors can progress throughout the recovery process. Considerable controversy exists with respect to sugar intake and obesity There is general consensus indicating that sugar sucrose, fructose is not a direct cause of obesity , , however, other studies have linked sugar-sweetened beverages SSB to an increase in body weight in children and adults , Several reasons are offered to explain this discrepancy, but somehow SSB appears to be a special case.
First, it is possible that liquid calories are not compensated by a total decrease in energy intake. Second, ingestion of SSB might be an indicator of unhealthy lifestyle None of these studies have linked SSB to sugar addiction so we cannot adequately assess the direct impact of compulsive SSB consumption on body weight.
As mentioned, this transition in diet is coupled with the obesity epidemic observed in developing countries , Similarly, a shift from minimally processed foods to ultra-processed more added sugar, more saturated fat, more sodium, less fiber food has been seen in Brazil This approach must be parallel to education programs. While ecological approaches targeting global nutrition policy appear promising, agricultural systems remain directed by multibillion-dollar multinational food corporations rather than by governments. It is difficult to predict how emerging data on FA can impact policy, particularly given that corporations have fiduciary responsibilities to their shareholders which require them to maximize profits and may compromise other social and ecological goals Some public health experts propose that we will need to address food corporations similarly to how the tobacco industry was addressed in recent years, with interdiction and litigation It remains unclear how an understanding of FA will translate to behavior change, however, a recent survey suggests that framing certain foods as addictive may increase obesity-related policy support such as warning labels, similar to tobacco Other researchers believe that sugar addiction is too narrow and therefore still premature, warning against policy changes that are unlikely to have an impact since sugar is already so ubiquitous in the food supply The FA theory directly implicates the food industry, while the nutrition transition theory implicates other global industries also potentially negatively impacting our environment.
We propose that the FA framework can lead to improved health outcomes but are more likely to be more pronounced in socially advantaged groups, given barriers created by socioeconomic status. Many public health interventions focused on obesity aim to reduce disparities between groups, which we believe can also have a meaningful impact on long-term health outcomes. Given the evidence reviewed herein, we make the case for sugar addiction in the animal model.
Overlooking these findings will represent a missed opportunity for obesity-related policy and a potential public health revolution. Potential treatment strategies for FA have been reviewed elsewhere A commentary on the necessity as well as potential downsides of the food addiction model was published previously The major assumption is that biochemistry drives behavior. The sugar addiction theory bridges current gaps between food science and neuroscience, and between nutrition and psychology. This theory was originally developed from animal studies, however there is no shortage of compelling human data.
There is a subtlety to food addiction where a significant majority of the people who meet criteria may not be aware of it, likely because it is not widely accepted as a social norm. A seminal paper by Glass and McAtee envisioned a future for public health which integrates the natural and behavioral sciences with respect to the study of health. These authors propose that next-generation models focus on how social environments affect the organism human which will affect the organs, cells, sub-cellular, and molecular levels, and how these will provide feedback at multiple levels.
To date the YFAS is the only validated measure to evaluate addiction-like eating.
Sugar Addiction: From Evolution to Revolution
More importantly, FA research has not been able to account for all of the social factors e. Additionally, FA is not limited to obesity, as this construct has been extended to non-obese populations which makes causal inference difficult to assess. Finally, there is strong evidence of the existence of sugar addiction, both at preclinical and clinical level. Our model has demonstrated that five out of eleven criteria for SUD are met, specifically: use of larger amounts and for longer than intended, craving, hazardous use, tolerance, and withdrawal. From an evolutionary perspective, we must consider addiction as a normal trait that permitted humans to survive primitive conditions when food was scarce.
As we evolved culturally, the neural circuits involved in addictive behaviors became dysfunctional and instead of helping us survive they are in fact compromising our health. All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. National Center for Biotechnology Information , U. Journal List Front Psychiatry v. Front Psychiatry.
Published online Nov 7. David A. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Psychosomatic Medicine, a section of the journal Frontiers in Psychiatry.
Received Apr 12; Accepted Oct The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
This article has been cited by other articles in PMC. Abstract The obesity epidemic has been widely publicized in the media worldwide. Keywords: obesity, food addiction, drug addiction, sucrose, feeding behavior, dopamine, acetylcholine, nucleus accumbens. Introduction Obesity has become one of the biggest health care burdens since the second World War ended, increasing morbidity and lowering life expectancy 1 , 2. Evolutionary and genetic aspects of feeding Adipose tissue in mammals play an important role in survival by preparing the body for periods of famine Evolution of addictive drugs When Charles Darwin postulated the evolution theory, he suggested that a trait would emerge if it contributed to survival and increase the reproductive success of a species.
Neural circuits for reward The limbic system consists of different brain regions engaged in various aspects of emotions. Dysfunction of the dopaminergic system in obese subjects Investigators can identify animals that have propensity to become obese in a 5-day weight gain on a high-fat diet OP rats Drugs of addiction and accumbens dopamine Most drugs of addiction activate the VTA-NAc pathway whether they are systemically injected or locally applied in the accumbens , Effect of drugs of abuse and withdrawal on acetylcholine release in the NAc Drugs of addiction exert differential responses on the accumbens cholinergic interneuron.
What is the difference between food and drugs of addiction? Can sugar be addictive? Table 1 Four broader categories for eleven criteria used for substance use disorder SUD. Impaired Control 1. Use larger amount and for longer than intended. Much time spent using. Social Impairment 1. Neglected major role to use. Activities given up to use.
- Is Sugar Really Addictive?.
- Case Studies in Vocal Pedagogy.
- Beating Sugar Addiction.
- Breaking The Devils Heart: A Logic of Demons Novel!
Continued use Despite Risk 1. Hazardous use. Pharmacologial Criteria 1. Open in a separate window. Additional aspects of sugar addiction are comparable to drug addiction So far, this model of sugar addiction meets five of the criteria established in the DSM Addiction potential of highly palatable food related to maternal influence Given ethical limitations, prospective studies examining the impact of extreme dietary imbalances high-sugar, or high-fat during human pregnancy cannot be undertaken.
Food addiction and eating disorders Research into the interaction between food addiction and eating disorders EDs , specifically binge eating disorder BED and bulimia nervosa BN , has led to conclusions of separate but related constructs. Sugar and obesity Considerable controversy exists with respect to sugar intake and obesity Policy implications While ecological approaches targeting global nutrition policy appear promising, agricultural systems remain directed by multibillion-dollar multinational food corporations rather than by governments. Author contributions All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.
Conflict of interest statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Footnotes Funding.
References 1. World Health Organization Obesity and Overweight. Fact Sheet Costs of foraging predispose animals to obesity-related mortality when food is constantly abundant. Perspective: a historical and scientific perspective of sugar and its relation with obesity and diabetes. Obesity: from the agricultural revolution to the contemporary pediatric epidemic. Congenit Heart Dis. Global, regional and national prevalence of overweight and obesity in children and adults a systematic analysis. Lancet — From undernutrition to overnutrition: the evolution of overweight and obesity among young men in Switzerland since the 19th century.
Obes Facts 9 — Obesity in britain: gluttony or sloth? Br Med J. Rising social inequalities in US childhood obesity, Ann Epidemiol. Physical activity, TV viewing, and weight in U. Obes Res. Physical inactivity, obesity, and type 2 diabetes: an evolutionary perspective. Res Q Exerc Sport 88 :1—8. Armelagos GJ. Brain evolution, the determinates of food choice, and the omnivore's dilemma.
Crit Rev Food Sci Nutr. Hall KD. Did the food environment cause the obesity epidemic? Obesity 26 — Nutrients 7 — Welsh JA, Figueroa J. Intake of added sugars during the early toddles period. Nutr Today 52 Suppl. Williamson DA. Obesity 25 — Food for thought: reward mechanisms and hedonic overeating in obesity. Curr Obes Rep.
Camacho S, Ruppel A. Is the calorie concept a real solution to the obesity epidemic? Glob Health Action 10 Aguirre M, Venema K. The art of targeting gut microbiota for tackling human obesity. Genes Nutr. Appetite self-regulation: environmental and policy influences on eating behaviors. Obesity 25 :S26— Can food and addiction change the game? Biol Psychiatry 73 —3. Popkin BM. Nutritional patterns and transitions. Popul Dev Rev. The nutrition transition: worldwide obesity dynamics and their determinants.
Nutrition transition and the global diabetes epidemic. Curr Diab Rep. Omran AR. The epidemiologic transition. A theory of the epidemiology of population change. Milbank Mem Fund Q 49 — Similarities between obesity in pets and children: the addiction model. Br J Nutr. Canaries in the coal mine: a cross-species analysis of the plurality of obesity epidemics. Black JL, Macinko J. Neighborhoods and obesity. Nutr Rev. The starvation-predation trade-off predicts trends in body size, muscularity, and adiposity between and within Taxa.
Am Nat. Food insecurity as a driver of obesity in humans: the insurance hypothesis. Behav Brain Sci. Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med. Ludwig DS. Technology, diet, and the burden of chronic disease. JAMA — Increasing consumption of ultra-processed foods and likely impact on human health. Evidence from Brazil. Public Health Nutr. Arq Bras Endocrinol Metabol. Sugar-sweetened beverages and genetic risk of obesity.
Interactions between genetics and sugar-sweetened beverage consumption on health outcomes: a review of gene-diet interaction studies. Front Endocrinol. Gene-nutrient interactions and susceptibility to human obesity. Intermittent access to a sucrose solution impairs metabolism in obesity-prone but not obesity-resistant mice. Physiol Behav. Melanocortin-4 receptor—regulated energy homeostasis. Nat Neurosci. Nutrigenetics and nutrigenomics of caloric restriction. Prog Mol Biol Transl Sci. Same genetic components underlie different measures of sweet taste preference. Am J Clin Nutr.
Sweet taste preferences are partly genetically determined: identification of a trait locus on chromosome Davis C. Subst Abuse Rehabil. Psychotropic substance-seeking: evolutionary pathology or adaptation? Addiction 97 — Evolution and the origins of disease. Sci Am. Pani L. Is there an evolutionary mismatch between the normal physiology of the human dopaminergic system and current environmental conditions in industrialized countries?
Mol Psychiatry 5 — Sugar addiction. Neurobiology of addiction versus drug use driven by lack of choice. Curr Opin Neurobiol. Front Psychiat. Papez J. A Proposed mechanisms of emotions. Arch Neurol Psychiat. Kalivas P, Volkow N. New medications for drug addiction hiding in glutamatergic neuroplasticity. Mol Psychiatry 16 — The neuroscience of natural rewards: relevance to addictive drugs. J Neurosci. What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Rev.
- Transition to Accrual Accounting: 9.
- The Corner Store (Revised)!
- Sweet attractions!
Di Chiara G. Nucleus accumbens shell and core dopamine: Differential role in behavior and addiction. Behav Brain Res. Homeostasis meets motivation in the battle to control food intake. Natural addiction: a behavioral and circuit model based on sugar addiction in rats. J Addict Med. Neurobiology of addiction: a neurocircuitry analysis. Lancet Psychiatry 3 — Reward, dopamine and the control of food intake: Implications for obesity.
7 Tips on How to Stop Eating So Much Sugar
Trends Cogn Sci. The dopamine motive system : implications for drug and food addiction. Nat Rev Neurosci. Brain dopamine and reward. Annu Rev Psychol. Salamone JD, Mercea C. The mysterious motivational functions of mesolimbic dopamine. Curr Opin Pharmacol. Pleasure systems in the brain. Neuron 86 —4. Nicola SM. Reassessing wanting and liking in the study of mesolimbic influence on food intake. Ungerstedt U. Adipsia and aphagia after 6-hydroxydopamine induced degeneration of the nigro-striatal dopamine system. Acta Physiol Scand Suppl.
Dopamine-deficient mice are severely hypoactive, adipsic, and aphagic. Cell 83 — Detecting behaviorally relevant changes in extracellular dopamine with microdialysis. Brain Res. Hernandez L, Hoebel BG. Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis. Life Sci. Accumbens dopamine and the regulation of effort in food-seeking behavior: modulation of work output by different ratio or force requirements.
Feeding and hypothalamic stimulation increase dopamine turnover in the accumbens. Effects of feeding and drinking on acetylcholine release in the nucleus accumbens, striatum, and hippocampus of freely behaving rats. J Neurochem. Eating and drinking cause increased dopamine release in the nucleus accumbens and ventral tegmental area in the rat: measurement by in vivo microdialysis. Neurosci Lett. Bassareo V, Di Chiara G.
Differential influence of associative and nonassociative learning mechanisms on the responsiveness of prefrontal and accumbal dopamine transmission to food stimuli in rats fed ad libitum. Neuroscience 89 — Hajnal A, Norgren R. Repeated access to sucrose augments dopamine turnover in the nucleus accumbens. Neuroreport 13 —6. Sham feeding corn oil increases accumbens dopamine in the rat. A conditioned stimulus decreases extracellular dopamine in the nucleus accumbens after the development of a learned taste aversion. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell.
Neuroscience — A high-fat meal, or intraperitoneal administration of a fat emulsion, increases extracellular dopamine in the nucleus accumbens. Brain Sci. Dopaminergic correlates of motivated behavior: importance of drive. Ahn S, Phillips AG. Dopaminergic correlates of sensory-specific satiety in the medial prefrontal cortex and nucleus accumbens of the rat. Schultz W. Reward functions of the basal ganglia. J Neural Transm. A neural substrate of prediction and reward. Science —9. Pattern of access determines influence of junk food diet on cue sensitivity and palatability.
Appetite — Central ghrelin induces feeding driven by energy needs not by reward. Neuroreport 18 —5. Gosnell BA. Central structures involved in opioid-induced feeding. Fed Proc. Stimulation of feeding by galanin: anatomical localization and behavioral specificity of this peptide's effects in the brain.
Peptides 11 — Galanin: stimulation of feeding induced by medial hypothalamic injection of this novel peptide. Eur J Pharmacol.
Overcoming a sweet tooth might be easier than you think.
Hypothalamic paraventricular injections of ghrelin: Effect on feeding and c-Fos immunoreactivity. Multiple brain sites sensitive to feeding stimulation by opioid agonists: a cannula-mapping study. Pharmacol Biochem Behav. Galanin in the hypothalamus raises dopamine and lowers acetylcholine release in the nucleus accumbens: a possible mechanism for hypothalamic initiation of feeding behavior. Opioids in the hypothalamus control dopamine and acetylcholine levels in the nucleus accumbens. Systemic administration of ghrelin increases extracellular dopamine in the shell but not the core subdivision of the nucleus accumbens.
Neurochem Int. Cholecystokinin combined with serotonin in the hypothalamus limits accumbens dopamine release while increasing acetylcholine: A possible satiation mechanism. Expression of ghrelin receptor mRNA in the rat and the mouse brain. J Comp Neurol. Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite.
J Clin Invest. Ghrelin increases the motivation to eat, but does not alter food palatability. Perello M, Dickson SL. Ghrelin signalling on food reward: a salient link between the gut and the mesolimbic system. J Neuroendocrinol. Modulation of feeding and drinking by dopamine in caudate and accumbens nuclei in rats. Indian J Exp Biol. Differential behavioral responses to dopaminergic stimulation of nucleus accumbens subregions in the rat. Sensitization and conditioning of feeding following multiple morphine microinjections into the nucleus accumbens.
Effects of selective dopamine D1 or D2 receptor blockade within nucleus accumbens subregions on ingestive behavior and associated motor activity. Does activation of midbrain dopamine neurons promote or reduce feeding? Int J Obes. Model for predicting and phenotyping at normal weight the long-term propensity for obesity in Sprague—Dawley rats. Evidence for defective mesolimbic dopamine exocytosis in obesity-prone rats.
How I Beat My Sugar Addiction - Carrots 'N' Cake
Reduced accumbens dopamine in Sprague-Dawley rats prone to overeating a fat-rich diet. Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity. Neuroscience —9. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science — Synapse 68 — Overlapping neuronal circuits in addiction and obesity : evidence of systems pathology. The D2 dopamine receptor gene as a determinant of reward deficiency syndrome. J R Soc Med. Neurogenetic impairments of brain reward circuitry links to Reward Deficiency Syndrome RDS : potential nutrigenomic induced dopaminergic activation.
J Genet Syndr Gene Ther. Dopamine genetics and function in food and substance abuse. Variation in the DRD2 gene affects impulsivity in intertemporal choice. Open J Psychiatry 3 — Optogenetically-induced tonic dopamine release from VTA-nucleus accumbens projections inhibits reward consummatory behaviors. Grace AA. Addiction 95 — Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Nicotine infused into the nucleus accumbens increases synaptic dopamine as measured by in vivo microdialysis.
Systemic nicotine-induced dopamine release in the rat nucleus accumbens is regulated by nicotinic receptors in the ventral tegmental area. Synapse 16 — Intracranial self-administration of morphine into the ventral tegmental area in rats. Endogenous opiate reward induced by an enkephalinase inhibitor, thiorphan, injected into the ventral midbrain.
Behav Neurosci. Localization of brain reinforcement mechanisms: intracranial self-administration and intracranial place-conditioning studies. Cocaine is self-administered into the shell region of the nucleus accumbens in Wistar rats. Ann N Y Acad Sci. Blunted dopamine transmission in addiction: potential mechanisms and implications for behavior.
Semin Nucl Med. How can drug addiction help us understand obesity? Effects of perinatal exposure to palatable diets on body weight and sensitivity to drugs of abuse in rats. Exposure to sucrose during periods of withdrawal does not reduce cocaine-seeking behavior in rats. Sci Rep. The distribution and compartmental organization of the cholinergic neurons in nucleus accumbens of the rat.
Neuroscience 31 — Characterization of cholinergic neurons in the rat neostriatum. A combination of choline acetyltransferase immunocytochemistry, Golgi-impregnation and electron microscopy. Neuroscience 12 —8. Immunocytochemical localization of choline acetyltransferase in rat ventral striatum: a light and electron microscopic study. J Neurocytol. Anticholinergics for symptomatic management of Parkinson's disease. Cochrane Database Syst Rev.
Roles of the M1 muscarinic acetylcholine receptor subtype in the regulation of basal ganglia function and implications for the treatment of Parkinson's Disease. J Pharmacol Exp Ther. Differential effect of systemic administration of bromocriptine and l-DOPA on the release of acetylcholine from striatum of intact and 6-OHDA-treated rats. Involvement of cholinergic system in hyperactivity in dopamine-deficient mice.
Neuropsychopharmacology 40 — The controversial case of biperiden from prescription drug to drug of abuse. J Clin Psychopharmacol. Dopaminergic activity of the antimuscarinic antiparkinsonian agents. Accumbens dopamine-acetylcholine balance in approach and avoidance. Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response.
Cholinergic modulation of mesolimbic dopamine function and reward. Supraadditive effect of d-fenfluramine plus phentermine on extracellular acetylcholine in the nucleus accumbens: possible mechanism for inhibition of excessive feeding and drug abuse. Accumbal cholinergic interneurons differentially influence motivation related to satiety signaling.
Extracellular acetylcholine is increased in the nucleus accumbens following the presentation of an aversively conditioned taste stimulus. Conditioned taste aversion from neostigmine or methyl-naloxonium in the nucleus accumbens. Microdialysis evidence that acetylcholine in the nucleus accumbens is involved in morphine withdrawal and its treatment with clonidine. Systemic morphine simultaneously decreases extracellular acetylcholine increases dopamine in the nucleus accumbens of freely moving rats. Neuropharmacology 30 — Morphine and naloxone, i.
Rada P, Hoebel BG. Acetylcholine in the accumbens is decreased by diazepam and increased by benzodiazepine withdrawal: a possible mechanism for dependency. Effects of nicotine and mecamylamine-induced withdrawal on extracellular dopamine and acetylcholine in the rat nucleus accumbens. Psychopharmacology — The influence of cocaine self-administration on in vivo dopamine and acetylcholine neurotransmission in rat caudate-putamen.
Different sensitivity of in vivo acetylcholine transmission to D1 receptor stimulation in shell and core of nucleus accumbens. Increased sensitivity to cocaine by cholinergic cell ablation in nucleus accumbens. In alcohol-treated rats, naloxone decreases extracellular dopamine and increases acetylcholine in the nucleus accumbens: evidence of opioid withdrawal. Acetylcholine enhancement in the nucleus accumbens prevents addictive behaviors of cocaine and morphine. Dopamine microdlalysis in the nucleus accumbens during acute and chronic morphine, naloxone-precipitated withdrawal and clonidine treatment.
Neuroanatomical specificity of conditioned responses to cocaine versus food in mice. Food addiction: clinical reality or mythology. Am J Med. Rogers P. Food and drug addiction: similarities and differences. Neurosci Biobehav Rev. Long-lasting deficits in hedonic and nucleus accumbens reactivity to sweet rewards by sugar overconsumption during adolescence. Eur J Neurosci. Reduced alcohol drinking in adult rats exposed to sucrose during adolescence.
Neuropharmacology 59 — Sugar overconsumption during adolescence selectively alters motivation and reward function in adult rats. Wei Z, Zhang X. Similarities and differences in diagnostic criterion. In Substance and Non-substance Addiction. Zhang X, editor. Singapore: Springer Nature; Sugar bingeing in rats.
Curr Protoc Neurosci. Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain. Neuroreport 12 — Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Pharmacological regulation of intravenous cocaine and heroin self-administration in rats: a variable dose paradigm.
You may experience slight physical discomfort, such as a headache, or cravings for sugar and carbs, but stick with the plan — this will pass. After a few days, you should notice improved physical well-being, less bloating, a clearer head, increased energy and improved mood. Could YOU be a sugar addict?
Share this article Share. Share or comment on this article: The 15 signs you could be a sugar addict e-mail More top stories. Bing Site Web Enter search term: Search. Hollyoaks star, 37, and husband David O'Mahony are expecting first child Gangland killings, family honour, illicit affairs Singer plants a kiss on wife on romantic picnic in LA park High-tech hotel that gets you fit - even in your sleep: Jogging underwater, electrically charged squats and The secret designer who makes Kate look great: Duchess donned her dresses for Wimbledon and Prince George's Why every midlife woman must watch their money when they fall in love: Ask his salary on the first date, And for our Next trick Sober October: Book expert Patricia Nicol recommends reading fictions about avoiding Or do you love a baby on a plane, too?
The one lesson I've learned from life: Anton du Beke says you shouldn't blame anyone except yourself Shh! Anti-agers no one but you need knot about: At 73, is it too late for me to have a facelift? My Lightbulb moment: Handbag designer Charlotte Jamme had her business idea while talking to other mothers This is what 54 looks like: Sandra Prince works in childcare, lives with her partner and has four daughters Maths quiz promises to test your knowledge of equations - but can YOU solve all 25 without a calculator?