The most important research discovery of the decade … There is a significant connection between diabetes and Parkinson’s
Are you tired all the time. Do you usually have little energy?
The breakdown of glucose synthesis may well be the reason. Metabolically, insulin receptors play a key role in the regulation of glucose homeostasis, Insulin signaling controls access to blood glucose in body cells.
Do you typically feel better in the morning before you have had something to eat? This is a clue that you may be susceptible to insulin resistance. Fasting over night means that is a 12 hour or more period you have not eaten anything. This is the condition needed by the body for the liver to manufacture ketones. Before eating anything in the morning. your brain is being efficiently fueled by ketones rather than glucose which is the by product of eating anything.
Epidemiological evidence and experimental data support the interaction between Parkinson’s and diabetes. Treatments for diabetes show promising neuro-protective results in PD patients for both diabetic and non-diabetic patients. Therefore, the role of anti-diabetic treatments for Parkinson’s patients offers a promising therapeutic approach.
Ask your self – why are so many persons diagnosed with neurological conditions so thin? A logical reason is that when they eat, their symptoms worsen, so they do not eat regularly
Studies that find the connection between diabetes and Parkinson’s
Mov Disord. 2022 Aug;37(8):1612-1623. The Impact of Type 2 Diabetes in Parkinson’s Disease. Dilan Athauda, James Evans, Anna Wernick, Gurvir Virdi, Minee L Choi, Michael Lawton, Nirosen Vijiaratnam, Christine Girges, Yoav Ben-Shlomo, Khalida Ismail, Huw Morris, Donald Grosset, Thomas Foltynie, Sonia Gandhi
Abstract
Background: Type 2 diabetes (T2DM) is an established risk factor for developing Parkinson’s disease (PD), but its effect on disease progression is not well understood.
Objective: The aim of this study was to investigate the influence of T2DM on aspects of disease progression in PD.
Methods: We analyzed data from the Tracking Parkinson’s study to examine the effects of comorbid T2DM on PD progression and quality of life by comparing symptom severity scores assessing a range of motor and nonmotor symptoms.
Results: We identified 167 (8.7%) patients with PD and T2DM (PD + T2DM) and 1763 (91.3%) patients with PD without T2DM (PD). After controlling for confounders, patients with Type 2 Diabetes had more severe motor symptoms, as assessed by Movement Disorder Society Unified Parkinson’s Disease Rating Scale, Part III (25.8 [0.9] vs. 22.5 [0.3] P = 0.002), and nonmotor symptoms, as assessed by Non-Motor Symptoms Scale total (38.4 [2.5] vs. 31.8 [0.7] P < 0.001), and were significantly more likely to report loss of independence (odds ratio, 2.08; 95% confidence interval [CI]: 1.34-3.25; P = 0.001) and depression (odds ratio, 1.62; CI: 1.10-2.39; P = 0.015). Furthermore, over time, patients with T2DM had significantly faster motor symptom progression (P = 0.012), developed worse mood symptoms (P = 0.041), and were more likely to develop substantial gait impairment (hazard ratio, 1.55; CI: 1.07-2.23; P = 0.020) and mild cognitive impairment (hazard ratio, 1.7; CI: 1.24-2.51; P = 0.002) compared with the PD group.
Conclusions: In the largest study to date, T2DM is associated with faster disease progression in Parkinson’s, highlighting an interaction between these two diseases. Because it is a potentially modifiable metabolic state, with multiple peripheral and central targets for intervention, it may represent a target for alleviating parkinsonian symptoms and slowing progression to disability and dementia.
Mov Disord. 2021 Jun;36(6):1420-1429. Type 2 Diabetes as a Determinant of Parkinson’s Disease Risk and Progression. Harneek Chohan, Konstantin Senkevich, Radhika K Patel, Jonathan P Bestwick, Benjamin M Jacobs, Sara Bandres Ciga, Ziv Gan-Or, Alastair J Noyce
Abstract
Background: Type 2 diabetes (T2DM) and Parkinson’s disease (PD) are prevalent diseases that affect an aging population. Previous systematic reviews and meta-analyses have explored the relationship between diabetes and the risk of PD, but the results have been conflicting.
Objective: The objective was to investigate T2DM as a determinant of PD through a meta-analysis of observational and genetic summary data.
Methods: A systematic review and meta-analysis of observational studies was undertaken by searching 6 databases. We selected the highest-quality studies investigating the association of T2DM with PD risk and progression. We then used Mendelian randomization (MR) to investigate the causal effects of genetic liability toward T2DM on PD risk and progression, using summary data derived from genome-wide association studies.
Results: In the observational part of the study, pooled effect estimates showed that T2DM was associated with an increased risk of PD (odds ratio [OR] 1.21, 95% confidence interval [CI] 1.07-1.36), and there was some evidence that T2DM was associated with faster progression of motor symptoms (standardized mean difference [SMD] 0.55, 95% CI 0.39-0.72) and cognitive decline (SMD -0.92, 95% CI -1.50 to -0.34). Using MR, we found supportive evidence for a causal effect of diabetes on PD risk (inverse-variance weighted method [IVW] OR 1.08, 95% CI 1.02-1.14; P = 0.010) and some evidence of an effect on motor progression (IVW OR 1.10, 95% CI 1.01-1.20; P = 0.032) but not on cognitive progression.
Conclusions: Using meta-analyses of traditional observational studies and genetic data, we observed convincing evidence for an effect of T2DM on PD risk and new evidence to support a role in PD progression.