Open access peer-reviewed chapter

Nutrition and Lifestyle Modifications in the Prevention and Treatment of Non-Alcoholic Fatty Liver Disease

By Kingsley Asare Kwadwo Pereko, Jacob Setorglo, Matilda Steiner- Asiedu and Joyce Bayebanona Maaweh Tiweh

Submitted: March 26th 2017Reviewed: September 29th 2017Published: March 21st 2018

DOI: 10.5772/intechopen.71368

Downloaded: 1015


Non-alcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide. NAFLD is an umbrella term for a range of liver conditions affecting people who drink little to no alcohol Different methods are employed in the diagnosis of NAFLD. Certain drugs, genetics, lifestyle factors have been implicated in the development of NAFLD. NAFLD symptoms are asymptomatic but indicated when there is unexplained persistent elevation of liver enzyme levels. Nutrition and lifestyle modifications are widely prescribed as helpful in the prevention and treatment of Non-Alcoholic Fatty Liver disease (NAFLD). Dietary and lifestyle modifications are apparent measures considering the disease association with obesity, diabetes, and cardiovascular disease which many reviews have linked to the condition. Reduction in body weight, involvement in both aerobic and anaerobic exercises, conscious intake in the types of fat and carbohydrates are helpful in the management of NAFLD. This chapter highlights the various theories and principles underlying nutrition and lifestyle modifications in the prevention and treatment of NAFLDs.


  • fatty liver
  • obesity
  • non-alcoholic
  • dietary
  • lifestyle

1. Introduction

Non-alcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and is a risk factor for both hepatic and cardiometabolic mortality [1, 2]. A meta-analysis of prevalence, incidence and outcome of NAFLD following publications on pubmed from 1989 to 2015 estimated global prevalence at 25.24% (95% CI: 22.10–28.65) with highest prevalence in the Middle East 31.79% (13.48–58.23) and South America 30.45% (22.74–39.44) and lowest in Africa 13.48% (5.69–28.69) [2]. NAFLD describes a range of conditions caused by a build-up of fat within liver cells and can be divided into four stages namely:

  1. Simple fatty liver (hepatic steatosis). Under normal conditions, very little fat is stored in liver cells of humans. Hepatic steatosis therefore refers to a situation where excess fat accumulates in the hepatic cells. Sometimes simple fatty liver does not cause any harm to the liver or pose health risks. However, in some instances it leads to NAFLD and its severe forms and that is where the problem arises.

  2. Non-alcoholic steatohepatitis (NASH). This expression is much less common than NAFLD. Here, the excess fat stored in the liver cells is associated with inflammation of the liver.

  3. Fibrosis: This is associated with persistent hepatitis, including steatohepatitis and may lead to scarring of the liver tissue (fibrosis). This is not life threatening since when fibrosis some of the liver cells that continue to perform its functions.

  4. Cirrhosis: This stage of a liver disease can be life threatening because normal liver tissues are replaced by a lot of fibrosis. The structure and function of the liver are therefore modified. There are different scientific means of detecting liver diseases.


2. Diagnosis

There are different methods of diagnosing NAFLD. The test ranges from metabolic syndrome assessment, detecting metabolites in the blood as well as enzymes such as Alanine transaminase (ALT) and Aspartate Aminotransferase (AST) [3]. Medical imaging and sonographic techniques are also performed to create an image of the liver. Further tests such as fibroscan and biopsy may be conducted apart from those listed earlier to determine the stage of the liver disease [4].


3. Risk factors

A wide range of diseases and conditions can predispose one to non-alcoholic fatty liver disease (NAFLD). Non-alcoholic steatohepatitis expresses itself among some sub-populations such as older people, diabetics and the obese. Certain drugs and hepatitis have been implicated in the development of NAFLD as well. Some risks are usually from lifestyle origin. These include:

  • High cholesterol and triglycerides levels,

  • Metabolic syndrome,

  • Central adiposity,

  • Polycystic ovary syndrome,

  • Sleep apnea,

  • Genetics,

  • Hypothyroidism,

  • Hypopituitarism [5].

Nutritional factors have also been cited as risks in the development of the disease. These include rapid weight loss, total parenteral nutrition, starvation and protein-calorie malnutrition [6]. The most common risk factor associated with NAFLD is the presence of the metabolic syndrome. The metabolic syndrome is defined by the presence of 3 or more of the following criteria (Table 1): (1) increased waist circumference, (2) hypertriglyceridemia, (3) hypertension, (4) high fasting glucose, and (5) a low high-density lipoprotein (HDL) level.

Impaired glucose toleranceFasting blood glucose level ≥ 110 mg/dL
High blood pressure≥130/85 mm Hg
Elevated triglyceride levels>250 mg/dL
Low high-density lipoprotein level<40 mg/dL for men;
<50 mg/dL for women
Abdominal obesityWaist: >102 cm (40 inches) for men;
>88 cm (35 inches) for women

Table 1.

Diagnostic criteria for metabolic syndrome.

Metabolic syndrome is diagnosed by the presence of 2 or more of these parameters.

Source: [2].


4. Signs and symptoms and management

Nonalcoholic fatty liver disease occurs in every age group but especially in people in their 40s and 50s. The condition is also closely linked to metabolic syndrome, which is a cluster of abnormalities including increased abdominal fat, poor ability to use the hormone insulin, high blood pressure and high blood levels of triglycerides. NAFLD symptoms are asymptomatic but indicated when there is unexplained persistent elevation of liver enzyme levels after hepatitis and other chronic liver diseases have been excluded. However, at certain stages of the disease, patients are malaise, fatigue, and right upper quadrant or diffuse abdominal discomfort. Hepatomegaly is found on clinical examination. When there is cirrhosis there may be; spider angiomata, ascites, splenomegaly, hard liver border, ascites, portal hypertension and jaundice or pruritus [7].

Clinical evaluation includes a careful history and physical examination. It is relevant to inquire about excess alcohol consumption which is defined as intakes greater than 30 g/day for men and greater than 20 g/day for women within the past 5 years. A drink is 350 mL (12 oz) of beer, 120 mL (4 oz) of wine, and 45 mL (1.5 oz) of hard liquor each contain 10 g of alcohol.

There are several approaches to managing NAFLD. Hepatoprotective therapy, antioxidants insulin-sensitizing agents and treatment of obesity are part of these. However, this text limits itself to the nutritional management of the NAFLD. Key to nutritional therapeutic procedures are lifestyle changes in diet and improving exercise habits in addition to the control of comorbidities which are secondary to the development of NAFLD [8]. For instance, bile acid derivatives and associated compounds that influence bile acid related are becoming prominent therapeutic agents for NAFLD [9, 10, 11]. The immediate associated lifestyle causes of NAFLD are targeted in the management of the disease condition.


5. Obesity and genetics

Obesity when combined with physical inactivity and genetic predisposition, has been directly associated with metabolic syndrome and NAFLD among some adult populations [12, 2]. Obesity itself is the failure of normal homeostatic regulation of energy utilization [9]. NAFLD can be a precursor to developing metabolic syndrome or insulin resistance [10]. Data suggest that about 80% of adults who are class 1 and/or 2 obese and 90% morbid obese according to the World Health Organization classification are at risk of having NAFLD [13]. Body weight loss can alter the cellular activity of adipose tissue and reverse many of the negative consequences of NAFLD. The excess fat and energy content of a meal has been associated with NAFLD development in healthy populations [14, 15]. Insulin resistance, oxidative stress, and cytokine toxicity results due to obesity and these factors have been implicated in the pathogenesis of NAFLD [16]. Among these factors, central adiposity and insulin resistance have direct association with hepatic fat content and visceral adiposity [17, 18, 19]. Polymorphisms (genetic variations) in the single-nucleotide polymorphisms (SNPs) T455C and C482T in APOC3 are associated with fatty liver disease. The carriers of T-455C, C-482 T, or both (not additive) had a 30% increase in fasting plasma apolipoprotein C3, 60% increase in fasting plasma triglyceride and 46% reduction in plasma triglyceride clearance. Oxidative stress, hormonal imbalances, and mitochondrial abnormalities can be potential causes.


6. Total fat

Dietary composition of a meal in terms of the macro-molecule distribution has a positive relation with the development of NAFLD. The amount and type of dietary fat may directly affect liver fat content, with high-fat diets being potentially harmful [20]. It has also been shown that a high ratio of omega-6 to omega-3 polyunsaturated fatty acids (PUFAs) and an increased intake of saturated and trans fatty acids are associated with NAFLD [21, 22, 23]. It was noted that when severely obese patients were fed diets containing higher percentage of total fat beyond recommended ranges, the risk of developing NALFD increased [24]. The deduction therefore was that the type of fat ingested rather than the amount is associated with NAFLD in obese individuals.


7. Saturated fatty acids

Saturated fatty acid component in meals has been shown to induce insulin resistance especially among the obese [25, 26, 27]. In epidemiologic studies, both total fat and saturated fat in the diet had significant correlation with triglyceride content in hepatic cells [28, 29]. In a double-blind randomized controlled trial of two reduced-fat diets, compared with a control diet both reduced-fat diets decreased amount of low density lipoprotein cholesterol (LDLc) in healthy males [30]. There was a decrease in high density lipoprotein cholesterol (HDLc) and increase in triglyceride levels increased with the reduced-fat diets. The authors concluded that reduced saturated fat intake (below 10%) may benefit patients with NAFLD. It was also observed that, low total fat and low saturated fat diet (23% fat and 7% saturated fat) predicted changes in HDLc and LDLc but not the amount of fat in the hepatocytes [31].


8. Transfatty acids

Trans fatty acids are positively associated with an increase in inflammatory processes, plasma triglycerides, and cholesterol as well as a reduction in HDLc level [32, 33]. Animal studies have shown positive relationships between the increased consumption of trans fatty acids from oxidized oils and liver inflammation [34, 35].


9. Polyunsaturated fatty acids (PUFAs)

Essential fatty acid, Omega-3 (which is a type of polyunsaturated fatty acids) PUFA levels are decreased in the hepatic tissue of people with NAFLD [22, 36] A higher omega-6 to omega-3 PUFA ratio may contribute to the development of a fatty liver within the hepatocytes of people NAFLD [36].


10. High carbohydrate intake

High carbohydrate intake especially the amount and type of carbohydrate consumed have an important impact on the development of NAFLD [37]. Simple carbohydrates intakes can lead to the development of NAFLD [38]. Meals high in carbohydrates lead to increased amounts of circulating insulin, which contribute to elevated triglyceride concentrations even under isocaloric conditions [39, 40]. A higher carbohydrate intake more than the recommended daily values has been positively associated with liver inflammation and NAFLD [24].

Coupled with a low-fat meal, high-carbohydrate meal promotes the development of a NAFLD through increased de novo fatty acid and triglyceride synthesis [41].

11. High-fructose corn syrup intake

Epidemiological data suggest that dietary pattern and an increased intake of simple sugars, especially fructose is associated with the development of NAFLD [42, 43]. The link is not too clear although it is assumed that the carbohydrates components increased risk of fatty infiltration of the liver or muscle. Therefore it was hypothesized that the link is through both indirect and direct mechanisms [44, 45]. Indirect association manifest itself through the adverse metabolic effects that can increase the risk of developing NAFLD. Fructose may cause hepatotoxic damage as a form of direct route link with NAFLD. Studies [46, 47, 48, 49] have suggested that increased fructose consumption augments fat mass, de novo lipogenesis, and inflammation. There is also induction of insulin resistance and fasting and postprandial triglycerides, which in turn, can result in liver steatosis. In other studies [50, 51], sugar-sweetened beverage consumption was found to be associated with fatty liver independent of body mass index of the individuals. Direct positive association was found between the amount of fructose consumed and the development of NAFLD [52, 53]. Age and frequency of consuming fructose-based food was also found to be related to liver inflammation and NAFLD [54].

12. Physical inactivity

Physical activity has been documented to improve health and hence the World Health Organization recommendations for aerobic an anaerobic exercises across the life span. Physical inactivity however, has been associated with NAFLD. Using matched controls for age and gender, only about one-fifth of individuals with NAFLD met recommendations for physical activity [55, 56]. Among 349 individuals studied, the NAFLD group engaged in less physical activity, including total, aerobic, and resistance [55].

It has been noted that decreased physical activity correlates with intra-hepatic fat, decreased cellular insulin sensitivity, and increased central adiposity [57, 58]. Sedentary time alone is associated with metabolic status. Sedentary times predicted higher levels of fasting insulin, independent of the amount of time spent engaging in moderate- or vigorous-intensity activity [59]. Therefore to improve metabolic health it is generally important to reduce sedentary lifestyle even when one meets the requirements for physical activity.

13. Treatments

Aggressive pursuit of modified lifestyle modifications coupled with dietary changes are critical in treating NAFLD when body weight is the underlying cause. That is because dietary macronutrient composition, physical activity, and all play critical roles in successful weight reduction. Weight loss is effective for improving NAFLD as it positively influences insulin sensitivity and dyslipidemia.

14. Body weight loss

It was found that about 9% body weight loss significantly improves NAFLD [60]. The result was thought to be due to improvements in inflammation and steatosis. Reduction in body weight through lowering of daily caloric intake of about 200 kcal/day improved liver cellular structure histology and enzymes function. A 10% body weight reduction resulted in a 45% reduction in liver fat content [61]. Lifestyle modification through dietary intake, exercise, and behavior modification with the guidelines from health experts has been show to lead to resolution in NALFD [62]. A weight reduction of about 7% was therefore recommended [63]. A combination of diet and exercise reduces fibrosis and amount of liver fat by an average of 40% [64, 65, 66]. The degree of hepatic fat reduction is related to the intensity of the lifestyle mediation and normally required a weight loss range of 5–10% is suggested.

15. Bariatric surgery

Among persons with higher grades of obesity, physical remedy such as reduction in dietary intake and physical activities does not result in resolution of NAFLD. Other means such as bariatric surgery is the most effective strategy to achieve and maintain weight loss [67]. Results from several uncontrolled studies [68, 69, 70] and controlled studies [71, 72] indicated that body weight loss achieved through bariatric surgery reduces amount of liver enzymes and improves NAFLD.

A study found an association between bariatric surgery and lower serum alanine transferase and aspartate aminotransferase levels at two and 10 years follow-up [73] and histological improvements [74]. Steatosis, steatohepatitis, and fibrosis improved among majority of patients that have undergone surgery [75]. It is worth noting that hepatic decompensation can occur after gastric bypass so decision to opt for this should be taken with great care [3].

16. Nutrient content and healthful fats

Dietary composition can directly manipulate NAFLD progress. Changing either the composition of the macronutrient or micronutrient content can directly affect the level of inflammation, amount of serum lipids and insulin resistance [49]. Inverse association was found between Mediterranean diet consumption and cardiovascular disease risk [76]. Among obese women and overweight men, a low-fat diet decreased hepatic fat compared with a high-fat diet [64, 77]. The dietary recommendation is that the diet contain less than 7% saturated fats, less than 1% of trans fats and 25–35% of the calorific intake should be total fat among which is polyunsaturated fatty acid.

17. Monounsaturated fats

It was found that replacing carbohydrate intake with monounsaturated fatty acids (MUFAs) to about 32 g/day increases triglyceride-rich lipoprotein catabolism [30]. This can lead to resolution of NAFLD. This finding is supported by epidemiological studies [31, 78]. Olive oil which contains about 73% MUFAs appears to provide a direct benefit in improving plasma lipids and possible NAFLD [79]. In randomized trials, [80, 81] isocaloric low-fat/high-carbohydrate diet improved hepatic fat and improved insulin sensitivity. The diet was composed of 50% MUFAs and 18% omega-3 PUFAs, 40% from carbohydrate, and 20% protein. These findings were independent of body weight loss of patients.

18. Omega-3 Omega-6 PUFAs

Evidence from epidemiologic and randomized controlled trials indicate that supplementation with omega-3 PUFAs lowers triglyceride levels and reduces the risk of coronary heart disease and mortality.94,95 High consumption of omega-3 PUFAs derived from fish diminishes hepatic triglyceride lipoprotein secretion and inhibits de novo lipogenesis. [82]. Using the Therapeutic Lifestyle Change diet criteria with a diet high in fish-derived omega-3 fatty acid (1.23 g/day EPA + DHA) vs. a low fish diet (0.27 g/day EPA + DHA) for 24 weeks, the higher fish diet decreased plasma triglycerides by 24%. Three human clinical trials support these findings by showing that giving patients with NAFLD omega-3 PUFAs (1 to 2.7 g/day for six to 12 months) improved hepatic steatosis, inflammation, and fibrosis [82, 83]. Capanni and Spadaro both demonstrated that triglyceride levels decreased 25 to 37 mg/dL when patients’ diets were supplemented with 1 to 2 g of omega-3 PUFAs per day for six and 12 months, respectively. This was thought to be through diminishes hepatic triglyceride lipoprotein secretion and inhibition de novo lipogenesis [82, 83, 84]. Diets based on therapeutic lifestyle change criteria supports improvements in NAFLD as the diet improves liver steatosis, inflammation, and fibrosis [85]. In a non-controlled trial, omega-6 PUFAs (15% of energy as linoleic acid) reduced liver fat compared with a diet high in saturated fatty acids in abdominally obese patients [86]. A diet consisting of mainly reduced simple carbohydrate may confer similar benefits among NALFD patients [87, 88].

19. Low sugar intake

Diet designed to produce a caloric deficit of 500 to1000 kcal/day is advised. Reduction of dietary carbohydrates, in particular dietary fructose, is the most beneficial and has been found to improve the lipid profile in overweight patients. Diets with less carbohydrate and more fat have relatively greater benefits in NAFLD management [89, 90]. Hypocaloric diet made up from 40% carbohydrate and 45% fat decreased serum alanine transaminase concentration than did a higher-carbohydrate (60%), low-fat diet (25% fat) [91]. Low-carbohydrate caloric restriction significantly improved hepatic insulin sensitivity. Diets with less carbohydrate and more fat have relatively greater benefits for insulin levels, triglycerides, and HDL cholesterol concentrations than do hypocaloric, low-fat diets. A hypocaloric diet moderately lower in carbohydrate (40% carbohydrate and 45% fat) decreased serum alanine transaminase concentrations to a greater degree than did a higher-carbohydrate, low-fat diet (60% carbohydrate and 25% fat).106 For individuals with NAFLD who were glucose intolerant, the low-carbohydrate caloric restriction significantly improved hepatic insulin sensitivity compared with the low-fat diet. In contrast, changes in visceral fat mass and insulin sensitivity were similar between a low-calorie, reduced-carbohydrate diet (fewer than 90 g of carbohydrate) and a reduced-fat diet (less than 20% fat). The World Health Organization recommends that the daily intake of added sugars makes up no more than 10% of total energy. The American Heart Association recommends limiting the amount of added sugars to no more than one-half of daily discretionary calories, which for women is approximately 100 kcal/day (6 tsp. of sugar) and for men is 150 kcal/day (9 tsp. of sugar).

20. Physical activity therapy

Physical activity enhances insulin sensitivity and favorably modifies lipids independent of weight loss [92, 93] Data suggest that there is improvement in cellular liver characteristics when NALFD individuals become active [94]. Exercise can lead to improvement in insulin sensitivity which intends contributes to the fatty acid delivery to the liver [95]. Improvement in insulin resistance and may decrease hepatic steatosis, inflammation, and disease progression in NAFLD [96, 97]. Four studies have investigated the effects of exercise without dietary modification on hepatic steatosis. Exercise can independently results in reduction in the fat in the hepatocytes without a significant weight change [98, 99, 100, 101].

21. Exercise intensity and duration

Both intermittent and daily exercise helps achieve weight loss and improve insulin sensitivity [102]. Intensity and duration contribute to energy expenditure and therefore can lead to insulin sensitivity, triglycerides, and serum glucose amount [103]. Vigorous exercise and doubling the duration of vigorous exercise was associated with decreased odds of developing fat in the liver [104]. Increased exercise by 60 minutes or more per week significantly reduced body weight and all liver enzymes [105]. Regular aerobic exercise for half an hour at least per day at 60–70% max heart rate for least 5 days per week reduces liver alanine transaminase levels [106].

22. Aerobic and resistance exercises

Increased aerobic exercise has been associated with improvement in the metabolic parameters associated with NAFLD [61, 94, 106]. Combined aerobic and resistance exercises have been shown to be more effective than aerobic exercise alone for resolving inflammation and cardiovascular risk factors [107]. An intervention of 30 minutes of aerobic exercise and 20 minutes of resistance exercise three times per week was found to be associated with improvements in hepatic fat among NAFLD patients [108]. This combination activity improves hepatic insulin sensitivity [100] reduction in liver fat [109]. Both findings were independent of body weight reduction. Antioxidant treatments such as vitamins and minerals supplementation have been mentioned to decrease oxidative stress and improve oxidative injury among NAFLD patients.

23. Vitamin E

In theory, vitamin E and other vitamins called antioxidants could help protect the liver by reducing or neutralizing the damage caused by inflammation. But more research is needed. Some evidence suggests vitamin E supplements may be helpful for people with liver damage caused by nonalcoholic fatty liver disease [110]. But vitamin E has been linked with increased risk of death and, in men, an increased risk of prostate cancer. Several small trials in humans with NAFLD have supported an effect of tocopherol (vitamin E) on the improvement of transaminase levels but there have been discordant results in histologic improvement [111]. There was a significant improvement in hepatic steatosis with vitamin E intakes at levels of 800 to 1000 IU/day [112, 113] Higher intakes of the vitamin can be fatal in most cases [114, 115].

24. Vitamin D

Vitamin D may play an important role in modifying the risk of cardio metabolic outcomes [116, 117]. Serum 25-hydroxy vitamin D concentrations were correlated with NAFLD in terms of liver steatosis, inflammation and fibrosis [118].

25. EPA + DHA

The evidence supporting the use of omega-3 PUFAs for treating NAFLD have consisted of small sample sizes and laden with errors [118, 119].

26. Probiotics

Gut microbiota has been associated with the development of obesity-related NAFLD [120]. Probiotics may improve liver enzymes and decrease markers of lipid peroxidation [121, 122]. The use of prebiotics and probiotics is to modify the microbiota as preventive or therapeutic strategies [123]. Their beneficial effects on NAFLD have been limited human studies [124]. Consuming a tablet containing 500 million Lactobacillus bulgaricusand Streptococcus thermophilusfor 3 months improved levels of liver enzyme in patients with NAFLD [124].

27. Other nutrients

Ginger (Zingiber officinale) can improve insulin sensitivity and reduce hepatic fat content [125]. In studies of people with non-alcoholic fatty liver disease, those who reported drinking coffee had less liver damage than those who drank little or no coffee. It’s not clear how coffee may influence liver damage or how much coffee you’d need to drink in order to benefit. Table 2 summarizes the nutritional guidelines in the management and treatment of NAFLD.

Weight loss10% of initial body weight over 6 months
Maintenance of weight loss
Bariatric surgery when individuals qualify
Calorie intake1200 to 1500 daily
*Energy deficit of 500 kcal/day based on Mifflin-St Jeor formula
Total fat≤ 35% of total calories
Monounsaturated fatty acids15–25% of total calories
Polyunsaturated fatty acids5–10% of total calories
Omega-3 fatty acids
Saturated fatty acids7–10% of total calories
Carbohydrate50% of total calories
> 50% carbohydrate sources from whole grains
Avoid high-fructose corn syrup
Added sugars <10% of total calories
Protein15% of total calories
Lean and vegetable protein
Physical activity≥ 150 minutes/week at moderate intensity or ≥75 minutes/week at vigorous intensity
Cardiovascular exercise five times weekly
Resistance training two or more times weekly
Decrease time spent sedentary

Table 2.

Guidelines in the management and treatment of NAFLD.

Source: [65, 81, 83].

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Kingsley Asare Kwadwo Pereko, Jacob Setorglo, Matilda Steiner- Asiedu and Joyce Bayebanona Maaweh Tiweh (March 21st 2018). Nutrition and Lifestyle Modifications in the Prevention and Treatment of Non-Alcoholic Fatty Liver Disease, Non-Alcoholic Fatty Liver Disease - Molecular Bases, Prevention and Treatment, Rodrigo Valenzuela, IntechOpen, DOI: 10.5772/intechopen.71368. Available from:

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