Advertisement

Journal of Neurology

, Volume 258, Issue 4, pp 613–617 | Cite as

Patients with elevated triglyceride and cholesterol serum levels have a prolonged survival in amyotrophic lateral sclerosis

  • J. Dorst
  • P. Kühnlein
  • C. Hendrich
  • J. Kassubek
  • A. D. Sperfeld
  • A. C. Ludolph
Original Communication

Abstract

Weight loss is a common phenomenon and an independent prognostic factor in amyotrophic lateral sclerosis (ALS). Several potential causal mechanisms, including intrinsic hypermetabolism and deficient food intake, have been discussed. We investigated the influence of fasting serum glucose, cholesterol, and triglyceride levels at time of diagnosis on survival in ALS. Serum cholesterol (LDL, HDL, and LDL/HDL ratio), triglycerides, and glucose were investigated in 488 patients (age of onset = 57.6 ± 12.6 years) in relation to survival and revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALS-FRS) data. High serum levels of both fasting cholesterol and triglycerides had a significantly positive effect on survival (p < 0.05). We found a median prolonged life expectancy by 14 months for patients with serum triglyceride levels above the median of 1.47 mmol/l. The results suggest that the lipid metabolism and the nutritional status of ALS patients are important prognostic factors. These parameters should be thoroughly monitored during the clinical management of these patients. In case of progressive loss of body weight, a diet rich in lipids and calories should be considered. However, the final decision whether a lipid-rich diet should be recommended to ALS patients can only be based on a double-blind placebo-controlled interventional trial. Our results further imply that lipid-lowering drugs, e.g., statins, should be applied carefully in ALS patients although individual risk considerations must be made.

Keywords

Amyotrophic lateral sclerosis Fat metabolism Nutrition 

References

  1. 1.
    Desport JC, Preux PM, Truong TC, Vallat JM, Sautereau D, Couratier P (1999) Nutritional status is a prognostic factor for survival in ALS patients. Neurology 53:1059–1063PubMedGoogle Scholar
  2. 2.
    Dupuis L, Oudart H, René F, Gonzalez De Aguilar JL, Loeffler JP (2004) Evidence for defective energy homeostasis in amyotrophic lateral sclerosis: benefit of a high-energy diet in a transgenic mouse model. Proc Natl Acad Sci USA 101(30):11159–11164PubMedCrossRefGoogle Scholar
  3. 3.
    Desport JC, Preux PM, Magy L, Boirie Y, Vallat JM, Beaufrère B, Couratier P (2001) Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis. Am J Clin Nutr 74(3):328–334PubMedGoogle Scholar
  4. 4.
    Dupuis L, Corcia P, Fergani A, Gonzalez De Aguilar JL, Bonnefont-Rousselot D, Bittar R, Seilhean D, Hauw JJ, Lacomblez L, Loeffler JP, Meininger V (2008) Dyslipidemia is a protective factor in amyotrophic lateral sclerosis. Neurology 70(13):1004–1009PubMedCrossRefGoogle Scholar
  5. 5.
    Chiò A, Calvo A, Ilardi A, Cavallo E, Moglia C, Mutani R, Palmo A, Galletti R, Marinou K, Pepetti L, Mora G (2009) Lower serum lipid levels are related to respiratory impairment in patients with ALS. Neurology 73(20):1681–1685PubMedCrossRefGoogle Scholar
  6. 6.
    Brooks BR, Miller RG, Swash M et al (2000) El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 1:293–299PubMedCrossRefGoogle Scholar
  7. 7.
    Neuhauser H, Ellert U (2008) Estimation of the metabolic syndrome prevalence in the general population in Germany. J Public Health 16:221–227CrossRefGoogle Scholar
  8. 8.
    Thomas L (1998) Blood glucose. In: Thomas L (ed) Clinical laboratory diagnostics. Use and assessment of clinical laboratory results. TH-Books Verlagsgesellschaft, Frankfurt/Main, pp 131–137Google Scholar
  9. 9.
    International Diabetes Federation Atlas (International Diabetes Federation, 2009)Google Scholar
  10. 10.
    Jawaid A, Murthy SB, Wilson AM et al (2010) A decrease in body mass index is associated with faster progression of motor symptoms and shorter survival in ALS. Amyotroph Lateral Scler (Epub ahead of print)Google Scholar
  11. 11.
    Saffer D, Morley J, Bill PL (1977) Carbohydrate metabolism in motor neuron disease. J Neurol Neurosurg Psychiatry 40:533–537PubMedCrossRefGoogle Scholar
  12. 12.
    Murai A, Miyahara T, Tanaka T, Kaneko T, Sako Y, Kameyama M (1983) Abnormalities of lipoprotein and carbohydrate metabolism in degenerative diseases of the nervous system–motor neuron disease and spinocerebellar degeneration. Tohoku J Exp Med 139(4):365–376PubMedCrossRefGoogle Scholar
  13. 13.
    Krentz AJ, Williams AC, Nattrass M (1991) Abnormal regulation of carbohydrate metabolism in motor neurone disease. Diabetes Res 16(2):93–99PubMedGoogle Scholar
  14. 14.
    Pradat PF, Bruneteau G, Gordon PH, Dupuis L, Bonnefont-Rousselot D, Simon D, Salachas F, Corcia P, Frochot V, Lacorte JM, Jardel C, Coussieu C, Forestier NL, Lacomblez L, Loeffler JP, Meininger V (2009) Impaired glucose tolerance in patients with amyotrophic lateral sclerosis. Amyotroph Lateral Scler 20:1–6CrossRefGoogle Scholar
  15. 15.
    Jawaid A, Salamone AR, Strutt AM, Murthy SB, Weaton M, McDowell EJ, Simpson E, Appel SH, York MK, Schulz PE (2010) ALS disease onset may occur later in patients with pre-morbid diabetes mellitus. Eur J Neurol 17:733–739PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  • J. Dorst
    • 1
  • P. Kühnlein
    • 1
  • C. Hendrich
    • 1
  • J. Kassubek
    • 1
  • A. D. Sperfeld
    • 1
  • A. C. Ludolph
    • 1
  1. 1.Department of NeurologyUniversity of UlmUlmGermany

Personalised recommendations