a balanced , effective macronutrient diet composition in gdm could improve maternal glycemia , but simultaneously could prevent worsening of maternal metabolic parameters that lead to excessive fetal growth . gdm has the potential to create a relentless cycle of obesity and diabetes prevalence . up to 50% of mothers with gdm moreover , the offspring of women with gdm are at risk for being large for gestational age ( lga ) ( 18 ) , having increased adiposity ( 19,20 ) , and developing impaired glucose tolerance ( 21,22 ) , metabolic syndrome ( 23 ) , and type 2 diabetes ( 15,16,2426 ) . strong positive associations between infant birth weight and later bmi support that larger newborns are more likely to become obese adults ( 18,27 ) , and females born lga ( 90th percentile ) have a doubled risk for delivering an lga infant themselves ( 28 ) . because the risk is attributed to in utero exposure to diabetes or gdm ( 26,29,30 ) , women with gdm perpetuate a cycle of obesity and diabetes prevalence through generations when affected daughters become pregnant ( 31 ) . overweight and obesity currently affect up to 75% of young women in the united states ( 32 ) , and , as gdm prevalence increases , the gdm intrauterine metabolic environment is expected to further fuel the risk of offspring obesity and glucose intolerance ( 33 ) . nutrition therapy holds great potential to effectively treat this growing population of mothers and offspring . a gdm diagnosis generates stress , anxiety , and fear , all of which may undermine any approach to nutrition therapy . until the diagnosis at 28 weeks gestation , most women have experienced a the diagnosis suddenly necessitates a high - risk pregnancy label , adherence to nutrition therapy , and heightened surveillance . anxiety and depression in these women may stem from self - blame ( 34 ) , feelings of loss of control ( 35,36 ) , fear of macrosomia or infant complications ( 36,37 ) , feelings of being misunderstood by their partner ( 38 ) , and fear of future type 2 diabetes ( 34 ) , all of which are magnified by the confining high - risk pregnancy label and controlled or restrictive nature of nutrition therapy ( 3638 ) . women with gdm have expressed feeling an intense moral obligation to the health of their unborn child , motivating them to endure intensified management ( 38 ) . although they are motivated to modify their lifestyle , adherence to nutrition therapy has been identified as the most arduous , confining component of treatment ( 34,36,37 ) . nutrition therapy has been described as intrusive ( 34 ) and an infringement on cultural / social roles , beliefs , and diet practices ( 35,36,39 ) . quick adaptation to a new diet composition late in pregnancy is challenging ( 34,40 ) . many women do not understand food properties ( i.e. , types of carbohydrates and types of fats ) , making food choices mentally taxing ( 40 ) . in our clinic , women with gdm were so fearful of macrosomia that they followed extreme carbohydrate - restricted diets , opting to replace calories from carbohydrates with calories from fat . although this practice resulted in controlled glycemia , mounting evidence supports a potential deleterious intrauterine programming effect of ffas on aberrant fetal growth and long - term infant health outcomes ( 41,42 ) . nutrition therapy is the first line of treatment for women with gdm . if effective , glycemia is controlled , and adequate weight gain and nutritional status are supported ( 12,43 ) . twenty years ago , it was reported based on clinical experience that a carbohydrate - restricted diet ( 40% ) in gdm blunted postprandial glucose excursions ( 8) . this observation fueled the focus on dietary carbohydrate and was corroborated when a strong association between maternal postprandial glycemia and infant size was reported ( 44,45 ) . although there is a rationale for carbohydrate restriction ( i.e. , glucose control ) , it also creates a context for unbalanced macronutrient intake . in obesogenic environments , a focus on carbohydrate restriction facilitates an increase in dietary fat due to the abundance and cost - effective availability of saturated fats and processed foods ( 46,47 ) . a large increase in protein is unlikely because it is consumed consistently in humans ( 46 ) . an unbalanced increase in protein ( i.e. , without appropriate micronutrient intake ) within pregnancy diets has been linked to reduced birth weight ( 48 ) . a diet - induced worsening of maternal insulin resistance ( 49,50 ) could further increase nutrient delivery to the fetus and worsen fetal hyperinsulinemia ( 51 ) . emerging data in animal and nonhuman primate models support an intrauterine influence of dietary fat in promoting offspring adiposity , hepatic steatosis , and metabolic syndrome ( 42,52 ) . in humans , maternal triglyceride and ffa levels may be stronger predictors of excess fetal fat accretion than maternal glucose ( 9,53 ) , raising the question of whether glycemia should constitute the only focus for therapy in gdm ( 54 ) . consensus panels , recognizing the metabolic impact of dietary macronutrients beyond carbohydrate , have withheld specific diet recommendations because of insufficient evidence ( 10 ) . despite the lack of evidence , the american college of obstetricians and gynecologists ( acog ) ( 5 ) and the endocrine society ( 55 ) still refer to carbohydrate restriction ( 3340% of total calories ) as the approach to treatment . mixed messages are conveyed to providers from consensus panels emphasizing glycemic and cardiometabolic health , within and outside of pregnancy ( table 1 ) . because women with gdm and their offspring are known to have heightened risk for type 2 diabetes and cardiovascular disease , overall glycemic and cardiovascular health are relevant considerations . for example , if a heart - healthy eating plan ( 56,57 ) can meet gdm management goals , it might also create an optimal intrauterine environment and a healthy long - term maternal postpartum nutritional pattern . although limiting carbohydrate can control glycemia , the influence of a carbohydrate - restricted , higher - fat diet in obese women with pre - pregnancy insulin resistance may unintentionally promote intrauterine overnutrition . comparison of nutrition therapy recommendations for gdm from professional health care organizations * for further comparison , recommendations from the ada for diabetes outside of pregnancy and from the aha / acc for cardiometabolic health outside of pregnancy are included . restriction of dietary carbohydrate has been the cornerstone of diabetes treatment for > 100 years . before insulin , a diet prescription of 8% carbohydrate and 70% fat nearly eliminated glycosuria ( 58 ) . early 20th century pioneers in diabetes management established that a low - carbohydrate diet prescription required individualization but is generally 40% of total calories ( 58 ) . as early management protocols for diabetes in pregnancy emerged to focus on  good  glycemic control to reduce maternal and fetal complications ( 59,60 ) , nutrition therapy for gdm evolved to focus on control of maternal glucose . data from later , nonrandomized trials supported carbohydrate restriction ( 61 ) by demonstrating blunted insulin secretion in response to a meal high in saturated fatty acids ( 62 ) and less need for insulin therapy with a carbohydrate intake < 42% ( 63 ) . however , carbohydrate restriction to < 39% has been linked to the highest infant birth weights ( 64 ) . most studies of nutrition therapy in gdm are riddled with confounding insulin use , lack of compliance , heterogeneity in outcome reporting , and the absence of reported infant outcomes ( i.e. , birth weight and body composition ) ( 11,12 ) . grounded in the concern about increased fat intake , we asked a question to challenge the dogma emphasizing carbohydrate restriction in gdm . what if nutrition therapy in gdm focused on liberalization of complex carbohydrate instead of restriction of all carbohydrate ? a salient finding across the few published randomized , controlled trials was that diets that were higher in complex carbohydrate and low in fact , in gdm , diets higher in unrefined / complex carbohydrate have effectively blunted postprandial glycemia ( 65,68 ) , reduced the need for insulin therapy ( 66 ) , lowered fasting ldl cholesterol levels ( 65,69 ) and ffas ( 65 ) , and improved insulin sensitivity ( 70 ) , a1c ( 69 ) , and systolic blood pressure ( 69 ) . thus , we developed a diet to challenge the low - carbohydrate diet for gdm ( 13 ) . we have named this diet choice ( choosing healthy options in carbohydrate energy ) , emphasizing an overall cardiometabolically healthy , nutrient - dense eating plan ( 57 ) that encourages choosing the right kinds of carbohydrate to control glycemia ( unrefined / complex / nutrient - dense ) , instead of restricting total carbohydrate . recently , we demonstrated in a controlled , randomized crossover study ( all food provided , diet - controlled gdm ) , that , compared to a low - carbohydrate diet ( 40% carbohydrate/45% fat ) , the choice diet ( 60% carbohydrate/25% fat ) effectively controlled glycemia to within current treatment targets ( 13 ) . although more high - quality , randomized studies are needed , all of the evidence to date suggests that liberalization of complex carbohydrate in nutrition therapy for gdm meets management goals , may be effective in optimizing maternal and infant metabolic outcomes , and may help mitigate rising insulin resistance with advancing gestation in women with diet - controlled gdm . might it be possible to mitigate adipose tissue insulin resistance using nutrition therapy in gdm ? if effective , this would result in optimal nutrient delivery and avoid the intrauterine overnutrition that programs aberrant growth patterns ( 42 ) . one of the greatest concerns in gdm is the risk for fetal lga status and increased adiposity , historically linked to maternal hyperglycemia ( 25,71 ) and recently confirmed ( 72,73 ) . it is now understood that maternal glucose , lipids ( triglycerides , ffas ) , and amino acids are all potent fuels for fetal growth . in normal late pregnancy , maternal insulin resistance increases to ensure rapidly increasing fetal - placental energy requirements and fetal growth . however , overweight and obese women who develop gdm enter pregnancy with chronic preexisting insulin resistance ( 74 ) and insufficient -cell reserve ( 1,3 ) . these women display worsened insulin resistance in skeletal muscle ( 75 ) , liver , and adipose tissue ( 2,3,76,77 ) by the third trimester . diets high in fat may promote insulin resistance in part through elevation of tumor necrosis factor  ( 78 ) and ffas , resulting in impaired insulin signaling ( 76,79 ) . elevated ffas may also promote a -cell defect ( 76 ) , and evidence suggests that higher pre- and early pregnancy intake of animal fats and cholesterol ( 80 ) are associated with increased risk for gdm , implicating an effect of dietary fat and cholesterol on exacerbation of insulin resistance . thus , there is concern that a low - carbohydrate diet that facilitates an unbalanced increase in fat may actually worsen maternal insulin resistance in gdm , contributing to intrauterine overnutrition . it serves as a suppressor of ffa release ( lipolysis ) from stored triglyceride in adipose tissue . with better insulin action , there is better insulin suppression of lipolysis , less ffa exposure over time , and improved tissue sensitivity to insulin . we have learned important lessons about diet and fuel metabolism from our controlled studies , both outside and within pregnancy . for example , after following a low - carbohydrate , high - fat diet ( 20 g carbohydrate / day ) for 6 weeks , men and women secreted minimal insulin over 24 hours , resulting in an almost complete lack of ffa suppression by insulin ( a marker of insulin resistance ) and sustained elevated ffa levels over 24 hours ( figure 1a and b ) ( 81 ) . our crossover study in diet - controlled gdm ( 13 ) showed that , after a controlled breakfast on the choice diet , there was a higher insulin response , resulting in lower postprandial ffas . the low - carbohydrate diet resulted in less insulin secretion ( as seen in our nonpregnant participants ) and worse suppression of lipolysis / increased postprandial ffas ( figure c and d ) . the case for complex carbohydrates in nutrition therapy for gdm : lessons from studies outside and within pregnancy . a and b. thirty - two healthy , obese subjects were admitted to the clinical translational research center ( ctrc ) after a 12-hour fast for a 24-hour feeding study during which blood was drawn hourly and meals were administered at regimented times ( indicated by arrows ; baseline diet composition 55% carbohydrate/30% fat ) . they were then randomly assigned to follow a carbohydrate - restricted , high - fat diet ( 20 g carbohydrate / day ; n = 16 ) or a calorie - restricted , low - fat / high - carbohydrate diet ( 55% carbohydrate/30% fat ; n = 16 ) for 6 weeks . the 24-hour feeding study was repeated 6 weeks later with meals matching the randomized diet composition . figure 1a shows reduced insulin secretion on the low - carbohydrate diet , and figure 1b shows the parallel lack of ffa suppression by insulin and sustained elevated ffas over 24 hours on the low - carbohydrate diet . c and d. in a randomized , crossover study , 16 women with diet - controlled gdm followed a conventional low - carbohydrate diet ( 40% carbohydrate/45% fat ) and the choice diet ( 60% carbohydrate/25% fat ) in random order for 3 days each ( gestational week 31 , 100% of calories provided , 2.5-day washout period between diets ) . on the fourth day of each diet treatment , women reported to the ctrc after an overnight fast . baseline samples were collected , and a standardized breakfast test meal matching the randomized diet composition was consumed . figure 1c shows the postprandial insulin response on choice , and figure 1d shows a parallel better suppression of postprandial ffas by choice . the low - carbohydrate diet resulted in less insulin secretion ( c ) but worse suppression of lipolysis and increased postprandial ffas ( d ) . humans are postprandial much of the day , and if the patterns seen in figures 1a and b were similar in mothers with gdm , there would be high fetoplacental lipid exposure over 24 hours on a low - carbohydrate diet . in diet - controlled gdm , if the responses in figures 1c and d were similar across meals , the low - carbohydrate diet would result in nearly 20% more lipid exposure than with the choice diet . importantly , early evidence also showed that 67 weeks of therapy with the choice diet resulted in lower fasting glucose and ffas , better insulin suppression of ffas in adipose tissue , less adipose tissue inflammation , and a trend for less neonatal adiposity , all of which suggest better insulin action despite the rising insulin resistance of pregnancy ( 82 ) . the case for including complex carbohydrates in nutrition therapy for gdm , then , is that , if the degree of maternal insulin resistance is a key regulator in controlling maternal glucose , lipids , and amino acids to the fetal - placental unit , and it can be lessened by balanced liberalization of complex nutrient - dense carbohydrate and reduced dietary fat , then excessive fetal growth and potential programming effects could be strongly modifiable by nutrition therapy in gdm . adherence to a low - carbohydrate diet is one of the most challenging components to therapy for gdm . it is possible that a less restrictive approach to nutrition therapy will lessen feelings of confinement in gdm . although more high - quality , randomized trials are needed , there is evidence that a balanced liberalization of complex carbohydrate as part of an overall nutrient - dense eating plan in gdm meets treatment goals and may mitigate maternal adipose tissue insulin resistance , both of which may promote optimal metabolic outcomes for mothers and their offspring .
in brief restriction of dietary carbohydrate has been the cornerstone for treatment of gestational diabetes mellitus ( gdm ) . 
 however , there is evidence that a balanced liberalization of complex carbohydrate as part of an overall eating plan in gdm meets treatment goals and may mitigate maternal adipose tissue insulin resistance , both of which may promote optimal metabolic outcomes for mother and offspring .