High Fat Diet Cause CFRD??

D

dramamama

New member
1: J Pediatr Gastroenterol Nutr. 2006 Nov;43(5):660-5. Links
Dietary and circulating polyunsaturated fatty acids in cystic fibrosis: are they related to clinical outcomes?

Colombo C,
Bennato V,
Costantini D,
Valmarana L,
Dacco V,
Zazzeron L,
Ghisleni D,
Bruzzese MG,
Scaglioni S,
Riva E,
Agostoni C.
Department of Pediatrics, CF Center, Fondazione IRCCS Policlinico, Mangiagalli, Regina Elena, University of Milan, Milan, Italy. carla.colombo@unimi.it
OBJECTIVE: To assess the relationship between dietary intakes, plasma phospholipid (PL) fatty acid profile and clinical parameters in children with cystic fibrosis (CF) in comparison to healthy controls. PATIENTS AND METHODS: A cross-sectional survey including 37 patients with CF (ages 8.0 +/- 2.9 yrs) and a reference group of 68 healthy children (ages 8.0 +/- 0.7 yrs) was carried out by means of a food-frequency questionnaire. At enrollment, all subjects underwent blood sampling for plasma PL fatty acids (FA). In CF patients, pulmonary function tests (forced expiratory volume in 1 second and forced vital capacity), anthropometric measurements and the Shwachman score were also determined. RESULTS: In CF patients, mean z score for weight and height (-0.35 +/- 1.16 and -0.28 +/- 0.99) were lower than controls (0.83 +/- 1.73 and 0.55 +/- 1.11, respectively). Patients with CF showed higher energy intakes (110 +/- 43 kcal/d) compared with controls (75 +/- 22 kcal/d; P < 0.0001), with higher intake of total (saturated and monounsaturated) fats and lower intake of polyunsaturated FA (3.9 +/- 1.0% of total macronutrient intake vs 4.3 +/- 1.2%, P = 0.05). In CF patients, plasma and PL levels of linoleic and docosahexaenoic acids were lower, whereas those of arachidonic acid were similar compared with controls. The Shwachman score showed significant positive associations with plasma PL levels of arachidonic acid and total n-6 long-chain FA (r = 0.32, P = 0.05, and r = 0.35, P = 0.03, respectively). CONCLUSIONS: <b>The data give suggestions that fat intake and CF-associated biomechanisms are bound in a vicious circle, concurring to create the clinical and biochemical picture of CF. The quantity and quality of fat supplementation in CF need careful attention to balance the fat supply with polyunsaturated FA.</b>

<b>Benefits
Polyunsaturated fat, along with monounsaturated fat are "healthy fats," the amount of which in one's daily diet should be near 45 g (in a 2000 calorie-per-day diet).[citation needed] Polyunsaturated fat can be found mostly in grain products, fish and sea food (herring, salmon, mackerel, halibut), soybeans, and fish oil. Foods like mayonnaise and soft margarine may also be good sources, but you should always check the nutritional label first. Polyunsaturated fat is necessary for the body and protects against illness[citation needed]. Omega-3 fatty acids in fish oil, fish and seafood lower the total amount of fat in the blood, which can lower blood pressure and decrease the risk of getting cardiovascular diseases.[1] Omega-6 fatty acids in sunflower oil and safflower oil also reduce the risk of cardiovascular disease, but can contribute to allergies and inflammation.[citation needed]
</b>
 
D

dramamama

New member
1: J Pediatr Gastroenterol Nutr. 2006 Nov;43(5):660-5. Links
Dietary and circulating polyunsaturated fatty acids in cystic fibrosis: are they related to clinical outcomes?

Colombo C,
Bennato V,
Costantini D,
Valmarana L,
Dacco V,
Zazzeron L,
Ghisleni D,
Bruzzese MG,
Scaglioni S,
Riva E,
Agostoni C.
Department of Pediatrics, CF Center, Fondazione IRCCS Policlinico, Mangiagalli, Regina Elena, University of Milan, Milan, Italy. carla.colombo@unimi.it
OBJECTIVE: To assess the relationship between dietary intakes, plasma phospholipid (PL) fatty acid profile and clinical parameters in children with cystic fibrosis (CF) in comparison to healthy controls. PATIENTS AND METHODS: A cross-sectional survey including 37 patients with CF (ages 8.0 +/- 2.9 yrs) and a reference group of 68 healthy children (ages 8.0 +/- 0.7 yrs) was carried out by means of a food-frequency questionnaire. At enrollment, all subjects underwent blood sampling for plasma PL fatty acids (FA). In CF patients, pulmonary function tests (forced expiratory volume in 1 second and forced vital capacity), anthropometric measurements and the Shwachman score were also determined. RESULTS: In CF patients, mean z score for weight and height (-0.35 +/- 1.16 and -0.28 +/- 0.99) were lower than controls (0.83 +/- 1.73 and 0.55 +/- 1.11, respectively). Patients with CF showed higher energy intakes (110 +/- 43 kcal/d) compared with controls (75 +/- 22 kcal/d; P < 0.0001), with higher intake of total (saturated and monounsaturated) fats and lower intake of polyunsaturated FA (3.9 +/- 1.0% of total macronutrient intake vs 4.3 +/- 1.2%, P = 0.05). In CF patients, plasma and PL levels of linoleic and docosahexaenoic acids were lower, whereas those of arachidonic acid were similar compared with controls. The Shwachman score showed significant positive associations with plasma PL levels of arachidonic acid and total n-6 long-chain FA (r = 0.32, P = 0.05, and r = 0.35, P = 0.03, respectively). CONCLUSIONS: <b>The data give suggestions that fat intake and CF-associated biomechanisms are bound in a vicious circle, concurring to create the clinical and biochemical picture of CF. The quantity and quality of fat supplementation in CF need careful attention to balance the fat supply with polyunsaturated FA.</b>

<b>Benefits
Polyunsaturated fat, along with monounsaturated fat are "healthy fats," the amount of which in one's daily diet should be near 45 g (in a 2000 calorie-per-day diet).[citation needed] Polyunsaturated fat can be found mostly in grain products, fish and sea food (herring, salmon, mackerel, halibut), soybeans, and fish oil. Foods like mayonnaise and soft margarine may also be good sources, but you should always check the nutritional label first. Polyunsaturated fat is necessary for the body and protects against illness[citation needed]. Omega-3 fatty acids in fish oil, fish and seafood lower the total amount of fat in the blood, which can lower blood pressure and decrease the risk of getting cardiovascular diseases.[1] Omega-6 fatty acids in sunflower oil and safflower oil also reduce the risk of cardiovascular disease, but can contribute to allergies and inflammation.[citation needed]
</b>
 
E

EnergyGal

New member
I wrote this article for this website in 2000.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.cysticfibrosis.com/personal_stories_full.cfm?article_id=100033
">http://www.cysticfibrosis.com/...cfm?article_id=100033
</a>
"I predict in the next ten years or sooner that there is going to be more education on the importance of eating quality foods for patients with CF. Educating parents will help to instill proper eating habits for their children. If proper education on eating quality foods could be emphasized presently, I believe that the lives of patients with CF would be extended and we would all lead a better quality of life. I wish that there were more patients who would be willing to participate in nutritional studies to prove nutritional theories. If you are patient who has CF and you feel that the foods that you eat are causing you discomfort than ask to speak to a nutritionist at your CF center. Try and keep a daily log of all the suspecting foods in your daily food intake. Discuss this with your Doctors and nutritionists. "

I guess I was right with my prediction. I never agreed with giving children with CF junk foods. We all might get CFRD one day BUT, It is my belief you can delay the onset of diabetes and prolong your life with a proper diet. Call your healthy diet whatever name you like, eating healthy and what AGREES with your own unique digestion system will work for you.

There are many other factors that go into helping your body to stay healthy, diet is one part of the picture.

If you have diabetes, you can improve your health by eating healthier. Perhaps you will still need insulin everyday, it is also possible that you will be taking less with improving your food choices as well as implementing an exercise program.

Going back to the original topic about Fats, I love eating AVOCADOS and use Olive Oil for my healthy fats.
 
E

EnergyGal

New member
I wrote this article for this website in 2000.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.cysticfibrosis.com/personal_stories_full.cfm?article_id=100033
">http://www.cysticfibrosis.com/...cfm?article_id=100033
</a>
"I predict in the next ten years or sooner that there is going to be more education on the importance of eating quality foods for patients with CF. Educating parents will help to instill proper eating habits for their children. If proper education on eating quality foods could be emphasized presently, I believe that the lives of patients with CF would be extended and we would all lead a better quality of life. I wish that there were more patients who would be willing to participate in nutritional studies to prove nutritional theories. If you are patient who has CF and you feel that the foods that you eat are causing you discomfort than ask to speak to a nutritionist at your CF center. Try and keep a daily log of all the suspecting foods in your daily food intake. Discuss this with your Doctors and nutritionists. "

I guess I was right with my prediction. I never agreed with giving children with CF junk foods. We all might get CFRD one day BUT, It is my belief you can delay the onset of diabetes and prolong your life with a proper diet. Call your healthy diet whatever name you like, eating healthy and what AGREES with your own unique digestion system will work for you.

There are many other factors that go into helping your body to stay healthy, diet is one part of the picture.

If you have diabetes, you can improve your health by eating healthier. Perhaps you will still need insulin everyday, it is also possible that you will be taking less with improving your food choices as well as implementing an exercise program.

Going back to the original topic about Fats, I love eating AVOCADOS and use Olive Oil for my healthy fats.
 
E

EnergyGal

New member
I wrote this article for this website in 2000.
<a target=_blank class=ftalternatingbarlinklarge href="http://www.cysticfibrosis.com/personal_stories_full.cfm?article_id=100033
">http://www.cysticfibrosis.com/...cfm?article_id=100033
</a>
"I predict in the next ten years or sooner that there is going to be more education on the importance of eating quality foods for patients with CF. Educating parents will help to instill proper eating habits for their children. If proper education on eating quality foods could be emphasized presently, I believe that the lives of patients with CF would be extended and we would all lead a better quality of life. I wish that there were more patients who would be willing to participate in nutritional studies to prove nutritional theories. If you are patient who has CF and you feel that the foods that you eat are causing you discomfort than ask to speak to a nutritionist at your CF center. Try and keep a daily log of all the suspecting foods in your daily food intake. Discuss this with your Doctors and nutritionists. "

I guess I was right with my prediction. I never agreed with giving children with CF junk foods. We all might get CFRD one day BUT, It is my belief you can delay the onset of diabetes and prolong your life with a proper diet. Call your healthy diet whatever name you like, eating healthy and what AGREES with your own unique digestion system will work for you.

There are many other factors that go into helping your body to stay healthy, diet is one part of the picture.

If you have diabetes, you can improve your health by eating healthier. Perhaps you will still need insulin everyday, it is also possible that you will be taking less with improving your food choices as well as implementing an exercise program.

Going back to the original topic about Fats, I love eating AVOCADOS and use Olive Oil for my healthy fats.
 
D

dramamama

New member
Just wanted to include the peer-reviewed article on the Med. Diet and CF. It does not explain how we can keep from getting cfrd by eating a Med.diet....However, I think the last line in the article is important..... Changing to the Med. diet is a starting place in helping the <b>cftr channel to function more effectively</b>. This is huge!!!

Unfortunately, the "picture" did not translate...I will happily email anyone the whole article.

British Journal of Nutrition (0007-1145) Volume 096(002), August 2006, pp 199-200
© The Authors, 2006
DOI: 10.1079/BJN20061815

Invited Commentary

Mediterranean diet and cystic fibrosis

Birgitta Strandvik MD, PhD1

1Department of Pediatrics, Institute of the Health of Women and Children, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden, birgitta.strandvik@pediat.gu.se

Abbreviations:

CF, cystic fibrosis

Low serum concentrations of linoleic acid were first documented in cystic fibrosis (CF) over 40 years ago (Kuo et al. 1962). For many years, these were considered to be a reflection of impaired fat absorption related to the pancreatic insufficiency present in 90 % of the patients. Low levels of essential fatty acids have, however, also been observed in patients without pancreatic insufficiency, indicating that the fatty acid disturbances are not solely a result of fat malabsorption (Underwood et al. 1972; Rogiers et al. 1983; Mischler et al. 1986). The development of more efficient pancreatic enzyme preparations that improve the fat absorption coefficient to above 90 % in many patients means that a malabsorption of essential fatty acids is not likely. However, a defective pattern of n-3 fatty acids has been described in such patients (Lloyd-Still et al. 1981). This received new attention when Freedman et al. (1999) described a restitution of pancreatic morphology by supplementation with high doses of DHA to Cftr?/? mice.

An increased release of arachidonic acid and an increased turnover of n-6 fatty acids have been found in many CF cell systems (Carlstedt-Duke et al. 1986; Levistre et al. 1993; Miele et al. 1997; Bhura-Bandali et al. 2000), including an overstimulation of phospholipase A2, the rate-limiting enzyme for arachidonic acid release (Berguerand et al. 1997). Since arachidonic acid release is the rate-limiting step in prostanoid synthesis, this overstimulation of phospholipase A2 results in a high production of eicosanoids (Strandvik et al. 1996). A high turnover would explain the low linoleic acid concentration (Fig. 1). It has been suggested that the low DHA concentration reflects a more basic defect of lipid metabolism in CF. However, linoleic acid supplementation normalises the concentration of DHA in serum (Farrell et al. 1985; Strandvik et al. 2001). It has recently also been shown that CF patients treated for 8 months with n-3 fatty acids showed an improvement in their linoleic acid concentration (De Vizia et al. 2003).

F1

Figure 1. Major series of fatty acids. Linoleic acid (LA) and ?-linolenic acid (ALA) are the essential fatty acids, which cannot be synthesised in mammals. Major metabolites of these fatty acids are arachidonic acid (AA), EPA and docosahexaenoic acid (DHA), respectively. In essential fatty acid deficiency, oleic acid (OA) is further metabolised to eicosatrienoic acid (mead acid). Substances in smaller letters indicate the pro- and anti-inflammatory products from AA, EPA and DHA, respectively.

In this context, the paper in this issue by Olveira et al. (2006) is of special interest. They report dietary intake and serum phospholipid fatty acids in adults with CF on a Mediterranean diet. The Spanish diet is richer in MUFA and also contains more n-3 fatty acids than a Western (American) diet (Simopoulos, 1999; Serra-Majem, 2003/2004). The patients in the present study were matched for age and sex with healthy controls, and a 7 d food registration disclosed a higher energy intake and a lower intake of n-6 essential fatty acids in the patients, suggesting a higher n-3:n-6 ratio in the patients' diet. Despite this favourable dietary profile, similar lipid abnormalities, as found by other authors, were seen. The authors excluded malabsorption as a major factor as their patients had a stable condition and the fat absorption coefficient, considered as the gold standard for fat absorption tests, was very good. Interestingly, they found significant differences in the lipid profile associated with the pancreatic and pulmonary functions and with the severity of the genotype, corroborating the results of previous studies (Lloyd-Still et al. 1996; Strandvik et al. 2001).

The patients reported were in a relatively good clinical state compared with many reports concerning adult patients in the US and Europe. This might be related to the fact that the Mediterranean diet contained a high fat content, thus supplying patients with CF with enough calories, and the lower n-6:n-3 ratio of the fat (Serra-Majem et al. 2003/2004). The present study shows, however, that a Mediterranean diet is not enough as these patients also need some kind of supplementation in order to normalise their fatty acid pattern.

The causal link between the lipid abnormality and CFTR dysfunction is not clear. There might be several possible explanations. The defect might be directly related to the CFTR through an unknown function of the protein comparable to those of other ABC cassette proteins, or indirectly related to its functioning in lipid membranes. CFTR resulting from the most common gene mutation, dF508, has been shown to have improved function at a lower temperature, suggesting that the lipid configuration around the protein might have importance for its function. Long-chain fatty acids are prone to lipid peroxidation, and an increased oxidative capacity in CF is well documented (Wood et al. 2001). In the paper by Olveira et al. (2006), the patients were supplemented with vitamin E and none was reported to have low serum concentrations. Although increased oxidation might contribute, it is highly unlikely to be a main cause of CF-related lipid abnormalities.

Linoleic acid is an important constituent of membranes, and the last step in the synthesis of DHA is dependent on normal membrane phospholipids in mitochondria and peroxisomes. Newly identified products of both arachidonic acid and DHA, lipoxins and resolvins, respectively, seem also to be involved in the pathophysiology of CF (Karp et al. 2005). Thus, the imbalance of lipid metabolism in CF will probably involve more metabolites than previously recognised. How to intervene in CF is still not clear (Beckles-Willson et al. 2002; Van Biervliet et al. 2005). A Mediterranean diet cannot compensate for the abnormalities, but it seems to be a solid ground for starting future interventions.

References

[R1] Beckles-Willson N Elliott T Everard ML (2002) Omega-3 fatty acids (from fish oils) for cystic fibrosis Cochrane Database of Systematic Reviews 2004 issue 3 CD002201

[R2] Berguerand M Klapisz E Thomas G Humbert L Jouniaux AM Olivier JL Bereziat G Masliah J (1997) Differential stimulation of cytosolic phospholipase A2 by bradykinin in human cystic fibrosis cell lines Am J Resp Cell Mol Biol 17 481 - 490

[R3] Bhura-Bandali FN Suh M Man SFP Clandinin MT (2000) The dF508 mutation in the cystic fibrosis transmembrane conductance regulator alters control of essential fatty acid utilization in epithelial cells J Nutr 130 2870 - 2875

[R4] Carlstedt-Duke J Brönnegård M Strandvik B (1986) Pathological regulation of arachidonic acid release in cystic fibrosis: the putative basic defect Proc Natl Acad Sci U S A 83 9202 - 9206

[R5] De Vizia B Raia V Spano C Pavlidis C Coruzzo A Alessio M (2003) Effect of an 8-month treatment with omega-3 fatty acids (eicosapentaenoic and docosahexaenoic) in patients with cystic fibrosis J Parent Ent Nutr 27 52 - 57

[R6] Farrell PM Mischler EH Engle MJ Brown J Lau SM (1985) Fatty acid abnormalities in cystic fibrosis Pediatr Res 19 104 - 109

[R7] Freedman SD Katz MH Parker EM Laposata M Urman MY Alvarez JG (1999) A membrane lipid imbalance plays a role in the phenotypic expression of cystic fibrosis in CFTR ?/? mice Proc Natl Acad Sci U S A 96 13995 - 14000

[R8] Karp CL Flick LM Yang R Uddin J Petasis NA (2005) Cystic fibrosis and lipoxins Prostaglandins Leukot Essent Fatty Acids 73 263 - 270

[R9] Kuo PT Huang NN Bassett DR (1962) The fatty acid composition of the serum chylomicrons and adipose tissue of children with cystic fibrosis of the pancrease J Pediatr 60 394 - 403

[R10] Levistre R Lemnaouar M Rybkine T Bereziat G Masliah J (1993) Increase of bradykinin stimulated arachidonic acid release in a delta-F508 cystic fibrosis epithelial cell line Biochim Biophys Acta 1181 233 - 239

[R11] Lloyd-Still JD Bibus DM Powers CA Johnson SB Holman RT (1996) Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis Acta Paediatr 85 1426 - 1432

[R12] Lloyd-Still JD Johnson SB Holman RT (1981) Essential fatty acid status in cystic fibrosis and the effects of safflower oil supplementation Am J Clin Nutr 34 1 - 7

[R13] Miele L Cordella-Miele E Xing M Frizell R Mukherjee AB (1997) Cystic fibrosis gene mutation (delta F508) is associated with an intrinsic abnormality in Ca2+?induced arachidonic acid release by epithelial cells DNA Cell Biol 16 749 - 759

[R14] Mischler EH Parrell SW Farrell PM Raynor WJ Lemen RJ (1986) Correction of linoleic acid deficiency in cystic fibrosis Pediatr Res 20 36 - 41

[R15] Olveira G Dorado A Olveira C Padilla A Rojo-Martinez G Garcia-Escobar E Gaspar I Gonzalo M Soriguer F (2006) Serum phospholipid fatty acid profile and dietary intake in an adult Mediterranean population with cystic fibrosis Br J Nutr 96 343 - 349

[R16] Rogiers V Vercruysse A Dab I Baran D (1983) Abnormal fatty acid pattern of the plasma cholesterol ester fraction in cystic fibrosis patients with and without pancreatic insufficiency Eur J Pediatr 141 39 - 42

[R17] Serra-Majem L Ngo de la Cruz J Ribas L Salleras L (2003/2004) Mediterranean diet and health: is all the secret in olive oil ? Pathophysiol Haemost Thromb 33 461 - 465

[R18] Simopoulos AP (1999) Essential fatty acids in health and chronic disease Am J Clin Nutr 70 560S - 569S

[R19] Strandvik B Gronowitz E Enlund F Martinsson T Wahlström J (2001) Essential fatty acid deficiency in relation to genotype in patients with cystic fibrosis J Pediatr 139 650 - 655

[R20] Strandvik B Svensson E Seyberth HW (1996) Prostanoid biosynthesis in patients with cystic fibrosis Prostaglandins Leukot Essent Fatty Acids 55 419 - 425

[R21] Underwood BA Denning CR Navab M (1972) Polyunsaturated fatty acids and tocopherol levels in patients with cystic fibrosis Ann NY Acad Sci 203 237 - 247

[R22] Van Biervliet S Van Biervliet JP Robberecht E Christophe A (2005) Docosahexaenoic acid trials in cystic fibrosis: A review of the rationale behind the clinical trials J Cyst Fibros 4 27 - 34

[R23] Wood LG Fitzgerald DA Gibson PG Cooper DM Collins CE Garg ML (2001) Oxidative stress in cystic fibrosis: dietary and metabolic factors J Am Coll Nutr 20 157 - 165

Top
 
D

dramamama

New member
Just wanted to include the peer-reviewed article on the Med. Diet and CF. It does not explain how we can keep from getting cfrd by eating a Med.diet....However, I think the last line in the article is important..... Changing to the Med. diet is a starting place in helping the <b>cftr channel to function more effectively</b>. This is huge!!!

Unfortunately, the "picture" did not translate...I will happily email anyone the whole article.

British Journal of Nutrition (0007-1145) Volume 096(002), August 2006, pp 199-200
© The Authors, 2006
DOI: 10.1079/BJN20061815

Invited Commentary

Mediterranean diet and cystic fibrosis

Birgitta Strandvik MD, PhD1

1Department of Pediatrics, Institute of the Health of Women and Children, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden, birgitta.strandvik@pediat.gu.se

Abbreviations:

CF, cystic fibrosis

Low serum concentrations of linoleic acid were first documented in cystic fibrosis (CF) over 40 years ago (Kuo et al. 1962). For many years, these were considered to be a reflection of impaired fat absorption related to the pancreatic insufficiency present in 90 % of the patients. Low levels of essential fatty acids have, however, also been observed in patients without pancreatic insufficiency, indicating that the fatty acid disturbances are not solely a result of fat malabsorption (Underwood et al. 1972; Rogiers et al. 1983; Mischler et al. 1986). The development of more efficient pancreatic enzyme preparations that improve the fat absorption coefficient to above 90 % in many patients means that a malabsorption of essential fatty acids is not likely. However, a defective pattern of n-3 fatty acids has been described in such patients (Lloyd-Still et al. 1981). This received new attention when Freedman et al. (1999) described a restitution of pancreatic morphology by supplementation with high doses of DHA to Cftr?/? mice.

An increased release of arachidonic acid and an increased turnover of n-6 fatty acids have been found in many CF cell systems (Carlstedt-Duke et al. 1986; Levistre et al. 1993; Miele et al. 1997; Bhura-Bandali et al. 2000), including an overstimulation of phospholipase A2, the rate-limiting enzyme for arachidonic acid release (Berguerand et al. 1997). Since arachidonic acid release is the rate-limiting step in prostanoid synthesis, this overstimulation of phospholipase A2 results in a high production of eicosanoids (Strandvik et al. 1996). A high turnover would explain the low linoleic acid concentration (Fig. 1). It has been suggested that the low DHA concentration reflects a more basic defect of lipid metabolism in CF. However, linoleic acid supplementation normalises the concentration of DHA in serum (Farrell et al. 1985; Strandvik et al. 2001). It has recently also been shown that CF patients treated for 8 months with n-3 fatty acids showed an improvement in their linoleic acid concentration (De Vizia et al. 2003).

F1

Figure 1. Major series of fatty acids. Linoleic acid (LA) and ?-linolenic acid (ALA) are the essential fatty acids, which cannot be synthesised in mammals. Major metabolites of these fatty acids are arachidonic acid (AA), EPA and docosahexaenoic acid (DHA), respectively. In essential fatty acid deficiency, oleic acid (OA) is further metabolised to eicosatrienoic acid (mead acid). Substances in smaller letters indicate the pro- and anti-inflammatory products from AA, EPA and DHA, respectively.

In this context, the paper in this issue by Olveira et al. (2006) is of special interest. They report dietary intake and serum phospholipid fatty acids in adults with CF on a Mediterranean diet. The Spanish diet is richer in MUFA and also contains more n-3 fatty acids than a Western (American) diet (Simopoulos, 1999; Serra-Majem, 2003/2004). The patients in the present study were matched for age and sex with healthy controls, and a 7 d food registration disclosed a higher energy intake and a lower intake of n-6 essential fatty acids in the patients, suggesting a higher n-3:n-6 ratio in the patients' diet. Despite this favourable dietary profile, similar lipid abnormalities, as found by other authors, were seen. The authors excluded malabsorption as a major factor as their patients had a stable condition and the fat absorption coefficient, considered as the gold standard for fat absorption tests, was very good. Interestingly, they found significant differences in the lipid profile associated with the pancreatic and pulmonary functions and with the severity of the genotype, corroborating the results of previous studies (Lloyd-Still et al. 1996; Strandvik et al. 2001).

The patients reported were in a relatively good clinical state compared with many reports concerning adult patients in the US and Europe. This might be related to the fact that the Mediterranean diet contained a high fat content, thus supplying patients with CF with enough calories, and the lower n-6:n-3 ratio of the fat (Serra-Majem et al. 2003/2004). The present study shows, however, that a Mediterranean diet is not enough as these patients also need some kind of supplementation in order to normalise their fatty acid pattern.

The causal link between the lipid abnormality and CFTR dysfunction is not clear. There might be several possible explanations. The defect might be directly related to the CFTR through an unknown function of the protein comparable to those of other ABC cassette proteins, or indirectly related to its functioning in lipid membranes. CFTR resulting from the most common gene mutation, dF508, has been shown to have improved function at a lower temperature, suggesting that the lipid configuration around the protein might have importance for its function. Long-chain fatty acids are prone to lipid peroxidation, and an increased oxidative capacity in CF is well documented (Wood et al. 2001). In the paper by Olveira et al. (2006), the patients were supplemented with vitamin E and none was reported to have low serum concentrations. Although increased oxidation might contribute, it is highly unlikely to be a main cause of CF-related lipid abnormalities.

Linoleic acid is an important constituent of membranes, and the last step in the synthesis of DHA is dependent on normal membrane phospholipids in mitochondria and peroxisomes. Newly identified products of both arachidonic acid and DHA, lipoxins and resolvins, respectively, seem also to be involved in the pathophysiology of CF (Karp et al. 2005). Thus, the imbalance of lipid metabolism in CF will probably involve more metabolites than previously recognised. How to intervene in CF is still not clear (Beckles-Willson et al. 2002; Van Biervliet et al. 2005). A Mediterranean diet cannot compensate for the abnormalities, but it seems to be a solid ground for starting future interventions.

References

[R1] Beckles-Willson N Elliott T Everard ML (2002) Omega-3 fatty acids (from fish oils) for cystic fibrosis Cochrane Database of Systematic Reviews 2004 issue 3 CD002201

[R2] Berguerand M Klapisz E Thomas G Humbert L Jouniaux AM Olivier JL Bereziat G Masliah J (1997) Differential stimulation of cytosolic phospholipase A2 by bradykinin in human cystic fibrosis cell lines Am J Resp Cell Mol Biol 17 481 - 490

[R3] Bhura-Bandali FN Suh M Man SFP Clandinin MT (2000) The dF508 mutation in the cystic fibrosis transmembrane conductance regulator alters control of essential fatty acid utilization in epithelial cells J Nutr 130 2870 - 2875

[R4] Carlstedt-Duke J Brönnegård M Strandvik B (1986) Pathological regulation of arachidonic acid release in cystic fibrosis: the putative basic defect Proc Natl Acad Sci U S A 83 9202 - 9206

[R5] De Vizia B Raia V Spano C Pavlidis C Coruzzo A Alessio M (2003) Effect of an 8-month treatment with omega-3 fatty acids (eicosapentaenoic and docosahexaenoic) in patients with cystic fibrosis J Parent Ent Nutr 27 52 - 57

[R6] Farrell PM Mischler EH Engle MJ Brown J Lau SM (1985) Fatty acid abnormalities in cystic fibrosis Pediatr Res 19 104 - 109

[R7] Freedman SD Katz MH Parker EM Laposata M Urman MY Alvarez JG (1999) A membrane lipid imbalance plays a role in the phenotypic expression of cystic fibrosis in CFTR ?/? mice Proc Natl Acad Sci U S A 96 13995 - 14000

[R8] Karp CL Flick LM Yang R Uddin J Petasis NA (2005) Cystic fibrosis and lipoxins Prostaglandins Leukot Essent Fatty Acids 73 263 - 270

[R9] Kuo PT Huang NN Bassett DR (1962) The fatty acid composition of the serum chylomicrons and adipose tissue of children with cystic fibrosis of the pancrease J Pediatr 60 394 - 403

[R10] Levistre R Lemnaouar M Rybkine T Bereziat G Masliah J (1993) Increase of bradykinin stimulated arachidonic acid release in a delta-F508 cystic fibrosis epithelial cell line Biochim Biophys Acta 1181 233 - 239

[R11] Lloyd-Still JD Bibus DM Powers CA Johnson SB Holman RT (1996) Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis Acta Paediatr 85 1426 - 1432

[R12] Lloyd-Still JD Johnson SB Holman RT (1981) Essential fatty acid status in cystic fibrosis and the effects of safflower oil supplementation Am J Clin Nutr 34 1 - 7

[R13] Miele L Cordella-Miele E Xing M Frizell R Mukherjee AB (1997) Cystic fibrosis gene mutation (delta F508) is associated with an intrinsic abnormality in Ca2+?induced arachidonic acid release by epithelial cells DNA Cell Biol 16 749 - 759

[R14] Mischler EH Parrell SW Farrell PM Raynor WJ Lemen RJ (1986) Correction of linoleic acid deficiency in cystic fibrosis Pediatr Res 20 36 - 41

[R15] Olveira G Dorado A Olveira C Padilla A Rojo-Martinez G Garcia-Escobar E Gaspar I Gonzalo M Soriguer F (2006) Serum phospholipid fatty acid profile and dietary intake in an adult Mediterranean population with cystic fibrosis Br J Nutr 96 343 - 349

[R16] Rogiers V Vercruysse A Dab I Baran D (1983) Abnormal fatty acid pattern of the plasma cholesterol ester fraction in cystic fibrosis patients with and without pancreatic insufficiency Eur J Pediatr 141 39 - 42

[R17] Serra-Majem L Ngo de la Cruz J Ribas L Salleras L (2003/2004) Mediterranean diet and health: is all the secret in olive oil ? Pathophysiol Haemost Thromb 33 461 - 465

[R18] Simopoulos AP (1999) Essential fatty acids in health and chronic disease Am J Clin Nutr 70 560S - 569S

[R19] Strandvik B Gronowitz E Enlund F Martinsson T Wahlström J (2001) Essential fatty acid deficiency in relation to genotype in patients with cystic fibrosis J Pediatr 139 650 - 655

[R20] Strandvik B Svensson E Seyberth HW (1996) Prostanoid biosynthesis in patients with cystic fibrosis Prostaglandins Leukot Essent Fatty Acids 55 419 - 425

[R21] Underwood BA Denning CR Navab M (1972) Polyunsaturated fatty acids and tocopherol levels in patients with cystic fibrosis Ann NY Acad Sci 203 237 - 247

[R22] Van Biervliet S Van Biervliet JP Robberecht E Christophe A (2005) Docosahexaenoic acid trials in cystic fibrosis: A review of the rationale behind the clinical trials J Cyst Fibros 4 27 - 34

[R23] Wood LG Fitzgerald DA Gibson PG Cooper DM Collins CE Garg ML (2001) Oxidative stress in cystic fibrosis: dietary and metabolic factors J Am Coll Nutr 20 157 - 165

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D

dramamama

New member
Just wanted to include the peer-reviewed article on the Med. Diet and CF. It does not explain how we can keep from getting cfrd by eating a Med.diet....However, I think the last line in the article is important..... Changing to the Med. diet is a starting place in helping the <b>cftr channel to function more effectively</b>. This is huge!!!

Unfortunately, the "picture" did not translate...I will happily email anyone the whole article.

British Journal of Nutrition (0007-1145) Volume 096(002), August 2006, pp 199-200
© The Authors, 2006
DOI: 10.1079/BJN20061815

Invited Commentary

Mediterranean diet and cystic fibrosis

Birgitta Strandvik MD, PhD1

1Department of Pediatrics, Institute of the Health of Women and Children, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden, birgitta.strandvik@pediat.gu.se

Abbreviations:

CF, cystic fibrosis

Low serum concentrations of linoleic acid were first documented in cystic fibrosis (CF) over 40 years ago (Kuo et al. 1962). For many years, these were considered to be a reflection of impaired fat absorption related to the pancreatic insufficiency present in 90 % of the patients. Low levels of essential fatty acids have, however, also been observed in patients without pancreatic insufficiency, indicating that the fatty acid disturbances are not solely a result of fat malabsorption (Underwood et al. 1972; Rogiers et al. 1983; Mischler et al. 1986). The development of more efficient pancreatic enzyme preparations that improve the fat absorption coefficient to above 90 % in many patients means that a malabsorption of essential fatty acids is not likely. However, a defective pattern of n-3 fatty acids has been described in such patients (Lloyd-Still et al. 1981). This received new attention when Freedman et al. (1999) described a restitution of pancreatic morphology by supplementation with high doses of DHA to Cftr?/? mice.

An increased release of arachidonic acid and an increased turnover of n-6 fatty acids have been found in many CF cell systems (Carlstedt-Duke et al. 1986; Levistre et al. 1993; Miele et al. 1997; Bhura-Bandali et al. 2000), including an overstimulation of phospholipase A2, the rate-limiting enzyme for arachidonic acid release (Berguerand et al. 1997). Since arachidonic acid release is the rate-limiting step in prostanoid synthesis, this overstimulation of phospholipase A2 results in a high production of eicosanoids (Strandvik et al. 1996). A high turnover would explain the low linoleic acid concentration (Fig. 1). It has been suggested that the low DHA concentration reflects a more basic defect of lipid metabolism in CF. However, linoleic acid supplementation normalises the concentration of DHA in serum (Farrell et al. 1985; Strandvik et al. 2001). It has recently also been shown that CF patients treated for 8 months with n-3 fatty acids showed an improvement in their linoleic acid concentration (De Vizia et al. 2003).

F1

Figure 1. Major series of fatty acids. Linoleic acid (LA) and ?-linolenic acid (ALA) are the essential fatty acids, which cannot be synthesised in mammals. Major metabolites of these fatty acids are arachidonic acid (AA), EPA and docosahexaenoic acid (DHA), respectively. In essential fatty acid deficiency, oleic acid (OA) is further metabolised to eicosatrienoic acid (mead acid). Substances in smaller letters indicate the pro- and anti-inflammatory products from AA, EPA and DHA, respectively.

In this context, the paper in this issue by Olveira et al. (2006) is of special interest. They report dietary intake and serum phospholipid fatty acids in adults with CF on a Mediterranean diet. The Spanish diet is richer in MUFA and also contains more n-3 fatty acids than a Western (American) diet (Simopoulos, 1999; Serra-Majem, 2003/2004). The patients in the present study were matched for age and sex with healthy controls, and a 7 d food registration disclosed a higher energy intake and a lower intake of n-6 essential fatty acids in the patients, suggesting a higher n-3:n-6 ratio in the patients' diet. Despite this favourable dietary profile, similar lipid abnormalities, as found by other authors, were seen. The authors excluded malabsorption as a major factor as their patients had a stable condition and the fat absorption coefficient, considered as the gold standard for fat absorption tests, was very good. Interestingly, they found significant differences in the lipid profile associated with the pancreatic and pulmonary functions and with the severity of the genotype, corroborating the results of previous studies (Lloyd-Still et al. 1996; Strandvik et al. 2001).

The patients reported were in a relatively good clinical state compared with many reports concerning adult patients in the US and Europe. This might be related to the fact that the Mediterranean diet contained a high fat content, thus supplying patients with CF with enough calories, and the lower n-6:n-3 ratio of the fat (Serra-Majem et al. 2003/2004). The present study shows, however, that a Mediterranean diet is not enough as these patients also need some kind of supplementation in order to normalise their fatty acid pattern.

The causal link between the lipid abnormality and CFTR dysfunction is not clear. There might be several possible explanations. The defect might be directly related to the CFTR through an unknown function of the protein comparable to those of other ABC cassette proteins, or indirectly related to its functioning in lipid membranes. CFTR resulting from the most common gene mutation, dF508, has been shown to have improved function at a lower temperature, suggesting that the lipid configuration around the protein might have importance for its function. Long-chain fatty acids are prone to lipid peroxidation, and an increased oxidative capacity in CF is well documented (Wood et al. 2001). In the paper by Olveira et al. (2006), the patients were supplemented with vitamin E and none was reported to have low serum concentrations. Although increased oxidation might contribute, it is highly unlikely to be a main cause of CF-related lipid abnormalities.

Linoleic acid is an important constituent of membranes, and the last step in the synthesis of DHA is dependent on normal membrane phospholipids in mitochondria and peroxisomes. Newly identified products of both arachidonic acid and DHA, lipoxins and resolvins, respectively, seem also to be involved in the pathophysiology of CF (Karp et al. 2005). Thus, the imbalance of lipid metabolism in CF will probably involve more metabolites than previously recognised. How to intervene in CF is still not clear (Beckles-Willson et al. 2002; Van Biervliet et al. 2005). A Mediterranean diet cannot compensate for the abnormalities, but it seems to be a solid ground for starting future interventions.

References

[R1] Beckles-Willson N Elliott T Everard ML (2002) Omega-3 fatty acids (from fish oils) for cystic fibrosis Cochrane Database of Systematic Reviews 2004 issue 3 CD002201

[R2] Berguerand M Klapisz E Thomas G Humbert L Jouniaux AM Olivier JL Bereziat G Masliah J (1997) Differential stimulation of cytosolic phospholipase A2 by bradykinin in human cystic fibrosis cell lines Am J Resp Cell Mol Biol 17 481 - 490

[R3] Bhura-Bandali FN Suh M Man SFP Clandinin MT (2000) The dF508 mutation in the cystic fibrosis transmembrane conductance regulator alters control of essential fatty acid utilization in epithelial cells J Nutr 130 2870 - 2875

[R4] Carlstedt-Duke J Brönnegård M Strandvik B (1986) Pathological regulation of arachidonic acid release in cystic fibrosis: the putative basic defect Proc Natl Acad Sci U S A 83 9202 - 9206

[R5] De Vizia B Raia V Spano C Pavlidis C Coruzzo A Alessio M (2003) Effect of an 8-month treatment with omega-3 fatty acids (eicosapentaenoic and docosahexaenoic) in patients with cystic fibrosis J Parent Ent Nutr 27 52 - 57

[R6] Farrell PM Mischler EH Engle MJ Brown J Lau SM (1985) Fatty acid abnormalities in cystic fibrosis Pediatr Res 19 104 - 109

[R7] Freedman SD Katz MH Parker EM Laposata M Urman MY Alvarez JG (1999) A membrane lipid imbalance plays a role in the phenotypic expression of cystic fibrosis in CFTR ?/? mice Proc Natl Acad Sci U S A 96 13995 - 14000

[R8] Karp CL Flick LM Yang R Uddin J Petasis NA (2005) Cystic fibrosis and lipoxins Prostaglandins Leukot Essent Fatty Acids 73 263 - 270

[R9] Kuo PT Huang NN Bassett DR (1962) The fatty acid composition of the serum chylomicrons and adipose tissue of children with cystic fibrosis of the pancrease J Pediatr 60 394 - 403

[R10] Levistre R Lemnaouar M Rybkine T Bereziat G Masliah J (1993) Increase of bradykinin stimulated arachidonic acid release in a delta-F508 cystic fibrosis epithelial cell line Biochim Biophys Acta 1181 233 - 239

[R11] Lloyd-Still JD Bibus DM Powers CA Johnson SB Holman RT (1996) Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis Acta Paediatr 85 1426 - 1432

[R12] Lloyd-Still JD Johnson SB Holman RT (1981) Essential fatty acid status in cystic fibrosis and the effects of safflower oil supplementation Am J Clin Nutr 34 1 - 7

[R13] Miele L Cordella-Miele E Xing M Frizell R Mukherjee AB (1997) Cystic fibrosis gene mutation (delta F508) is associated with an intrinsic abnormality in Ca2+?induced arachidonic acid release by epithelial cells DNA Cell Biol 16 749 - 759

[R14] Mischler EH Parrell SW Farrell PM Raynor WJ Lemen RJ (1986) Correction of linoleic acid deficiency in cystic fibrosis Pediatr Res 20 36 - 41

[R15] Olveira G Dorado A Olveira C Padilla A Rojo-Martinez G Garcia-Escobar E Gaspar I Gonzalo M Soriguer F (2006) Serum phospholipid fatty acid profile and dietary intake in an adult Mediterranean population with cystic fibrosis Br J Nutr 96 343 - 349

[R16] Rogiers V Vercruysse A Dab I Baran D (1983) Abnormal fatty acid pattern of the plasma cholesterol ester fraction in cystic fibrosis patients with and without pancreatic insufficiency Eur J Pediatr 141 39 - 42

[R17] Serra-Majem L Ngo de la Cruz J Ribas L Salleras L (2003/2004) Mediterranean diet and health: is all the secret in olive oil ? Pathophysiol Haemost Thromb 33 461 - 465

[R18] Simopoulos AP (1999) Essential fatty acids in health and chronic disease Am J Clin Nutr 70 560S - 569S

[R19] Strandvik B Gronowitz E Enlund F Martinsson T Wahlström J (2001) Essential fatty acid deficiency in relation to genotype in patients with cystic fibrosis J Pediatr 139 650 - 655

[R20] Strandvik B Svensson E Seyberth HW (1996) Prostanoid biosynthesis in patients with cystic fibrosis Prostaglandins Leukot Essent Fatty Acids 55 419 - 425

[R21] Underwood BA Denning CR Navab M (1972) Polyunsaturated fatty acids and tocopherol levels in patients with cystic fibrosis Ann NY Acad Sci 203 237 - 247

[R22] Van Biervliet S Van Biervliet JP Robberecht E Christophe A (2005) Docosahexaenoic acid trials in cystic fibrosis: A review of the rationale behind the clinical trials J Cyst Fibros 4 27 - 34

[R23] Wood LG Fitzgerald DA Gibson PG Cooper DM Collins CE Garg ML (2001) Oxidative stress in cystic fibrosis: dietary and metabolic factors J Am Coll Nutr 20 157 - 165

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S

Sreh

New member
That is an interesting article, I would appreciate the full article emailed to me... at joxam@hotmail.com
Thanks.
 
S

Sreh

New member
That is an interesting article, I would appreciate the full article emailed to me... at joxam@hotmail.com
Thanks.
 
S

Sreh

New member
That is an interesting article, I would appreciate the full article emailed to me... at joxam@hotmail.com
Thanks.
 
B

batteredNfried

New member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>sakasuka</b></i>

CFRD is an issue, no doubt. And some CFers are so fat that they're getting Type II diabetes related to their weight. So you can go overboard, for sure.



I'd love to see the studies that this doc is presenting.</end quote></div>

Here's an abstract I found that relates CF and obesity. <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16182686">Overweight and Obese CF</a>
 
B

batteredNfried

New member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>sakasuka</b></i>

CFRD is an issue, no doubt. And some CFers are so fat that they're getting Type II diabetes related to their weight. So you can go overboard, for sure.



I'd love to see the studies that this doc is presenting.</end quote></div>

Here's an abstract I found that relates CF and obesity. <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16182686">Overweight and Obese CF</a>
 
B

batteredNfried

New member
<div class="FTQUOTE"><begin quote><i>Originally posted by: <b>sakasuka</b></i>

CFRD is an issue, no doubt. And some CFers are so fat that they're getting Type II diabetes related to their weight. So you can go overboard, for sure.



I'd love to see the studies that this doc is presenting.</end quote></div>

Here's an abstract I found that relates CF and obesity. <a target=_blank class=ftalternatingbarlinklarge href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16182686">Overweight and Obese CF</a>
 
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