Malaysian Palm Oil Council Research Articles

The Influence of Extrinsic Motivation and Cross-Cultural Adjustment on Foreign Worker Commitment: The Mediating Role of Cross-Cultural Adjustment and Moderating Role of Employer Trust

Palm oil is a key income source in Malaysia, with the industry heavily reliant on foreign workers. This reliance necessitates a focus on their welfare to address workforce shortages. This study examines the relationship between extrinsic motivation and organizational commitment, mediated by cross-cultural adjustment and moderated by employer trust among foreign workers. This study employed a quantitative research design, using SPSS for data analysis, and surveyed 242 foreign workers from companies listed on the Malaysian Palm Oil Council (MPOC) website in 2022, achieving a 100% response rate. The key findings show that organizational commitment positively influences extrinsic motivation, with cross-cultural adjustment significantly enhancing both. Employer trust moderates the relationship between organizational commitment and cross-cultural adjustment, underscoring its importance in cultural adaptation and motivation. These insights highlight the need for targeted strategies to improve job satisfaction and retention among foreign workers by addressing extrinsic motivational factors and cultural adaptation challenges. The research contributes to the literature by detailing the interplay of organizational factors and cultural adaptation in shaping motivational outcomes, suggesting future research to explore longitudinal studies and other moderating variables. These findings offer valuable implications for improving workforce performance and retention strategies in the palm oil industry.

A COMPARATIVE STUDY BETWEEN UNIVARIATE AND BIVARIATE TIME SERIES MODELS FOR CRUDE PALM OIL INDUSTRY IN PENINSULAR MALAYSIA

The main purpose of this study is to compare the performances of univariate and bivariate models on four time series variables of the crude palm oil industry in Peninsular Malaysia. The monthly data for the four variables, which are the crude palm oil production, price, import and export, were obtained from Malaysian Palm Oil Board (MPOB) and Malaysian Palm Oil Council (MPOC). In the first part of this study, univariate time series models, namely, the autoregressive integrated moving average (ARIMA), fractionally integrated autoregressive moving average (ARFIMA) and autoregressive autoregressive (ARAR) algorithm were used for modelling and forecasting purposes. Subsequently, the dependence between any two of the four variables were checked using the residuals’ sample cross correlation functions before modelling the bivariate time series. In order to model the bivariate time series and make prediction, the transfer function models were used. The forecast accuracy criteria used to evaluate the performances of the models were the mean absolute error (MAE), root mean square error (RMSE) and mean absolute percentage error (MAPE). The results of the univariate time series showed that the best model for predicting the production was ARIMA while the ARAR algorithm were the best forecast models for predicting both the import and export of crude palm oil. However, ARIMA appeared to be the best forecast model for price based on the MAE and MAPE values while ARFIMA emerged the best model based on the RMSE value. When considering bivariate time series models, the production was dependent on import while the export was dependent on either price or import. The results showed that the bivariate models had better performance compared to the univariate models for production and export of crude palm oil based on the forecast accuracy criteria used.

Does The Crude Palm Oil Market Walk Randomly?

Study about the efficiency of the capital market has been extensively conducted, but it is still lack of research on the efficiency of other financial markets such as commodity markets. This study specifically examines market efficiency in a weak form in a commodity market, especially in the crude palm oil (CPO) market. The purpose of this research is to analyze the weak form efficiency of the CPO market. Data used in this research is monthly CPO closing price data in 2010-2017 from Bursa Malaysia Derivative Exchange (BMD). This data was obtained from the Malaysian Palm Oil Council (MPOC). The analysis tool used is Runs Test, following by Unit Root Test and Correlogram as robustness checking. The result of this study shows that the CPO market is being efficient in a weak form. This shows that CPO price walks randomly so that the technical analysis cannot be applied to predict the CPO price. The result of this study suggests to both of CPO traders, and CPO speculators in their transaction on BMD do not rely on technical analysis. JEL Classifications: G14; Q02 DOI: https://doi.org/10.26905/jkdp.v22i2.2023

Utilization of Palm Oil Fuel Ash and Rice Husks in Unfired Bricks for Sustainable Construction Materials Development

The production of sustainable construction component could prevent and control the pollution and environmental degradation in Malaysia. This is a key area in Malaysia’s Green Strategies (Ministry of Science, Technology and the environment, 2002). This paper reports on the laboratory investigation to establish the potential of utilizing Palm Oil Fuel Ash (POFA) and Rice Husk (RH) in developing green construction components. Malaysian Palm Oil Council (MPOC) reported that currently Malaysia’s contribution to world palm oil production is 39% and has taken 44% of world exports. Consequently it will increase the POFA production in palm oil manufacturing and this waste sometimes dispose in open area near the factory. On the other hand Malaysia also producing more 300k hectares of paddy production, thus rice husk is also a concern as an agricultural waste. The research objective is to study on the potential of utilizing of agricultural waste in developing of green bricks. This research involved laboratory investigations. In this research 2% - 10% of POFA and 1% - 5% RH were used in the mix composition of the brick’s weight. Addition of POFA was aimed to reduce the cement usage and RH was added to reduce sand in the bricks. The bricks were manually pressed in Materials Laboratory in Faculty of Architecture, Planning and Surveying, UiTM Shah Alam. The result showed that the addition of POFA and RH are able to reduce the density but in contrast the compressive strength were decrease compare to the control unit.

Abstract P3-03-11: Oxazine derivatives of g- and D- tocotrienols display potent anticancer effects in vivo

Abstract Breast cancer is a multi-stage process which leads to the accumulation of abnormal cells arising from excessive proliferation, lack of apoptosis or a combination of both. Natural compounds such as g-tocotrienol have been shown to selectively inhibit cancer cell growth without harming normal cell viability with little or no adverse side effects. The antiproliferative and apoptotic effects of the tocotrienol isoform, γ-tocotrienol, have been firmly established in various cancer types. However, in vivo studies have provided mixed results, attributed to γ-tocotrienol rapid clearance and low bioavailability. In order to improve anticancer potency and bioavailability in vivo, γ- and Δ-tocotrienol were chemically modified with electrophilic substitution reactions on their chromane ring using Mannich and Lederer-Manasse reactions, resulting in the synthesis of various oxazine derivatives. Several of these oxazine derivatives (compounds 26, 31, 39, 40 and 44) were found to display potent anticancer activity as compared to their parent compounds when tested on +SA mammary cancer cells grown in culture. These in vitro studies were followed up with in vivo studies to determine the anticancer effects of oxazine derivatives on the growth of mammary tumors in mice. Female syngeneic BALB/c mice, 4-6 week old were inoculated with 1×106 +SA mammary tumor cells in the left mammary pad. Once tumor size reached 5mm in diameter, animals were divided into different treatment groups and received an intra-tumoral injection injected of 0-120μg/20μl tocotrienol or its derivative every other day for 11 days. Afterwards, mice were sacrificed, tumors removed and placed in -80°C until further analysis. Results from these studies showed that tumor growth rate was significantly reduced in the oxazine derivative treated animals as compared to the vehicle-treated controls. Western blot analysis of tumor samples showed that the growth inhibitory effects of tocotrienol derivatives was also associated with a significant reduction in phosphorylated (activated) Akt and reductions in cell cycle regulatory proteins cyclin D1 and cyclin dependent kinases (CDK2, CDK4 and CDK6). In addition, oxazine derivative treatment was also associated with a large increase in CDK inhibitors p21 and p27, as compared to tumors obtained from the vehicle-treated control mice. Western blot analysis also showed that tumor from oxazine-derivative treated mice displayed a large reduction in NFκB levels and its downstream gene product COX-2. In summary, oxazine derivatives of tocotrienols display more potent anticancer activity both in vitro and in vivo, as compared to their parent compounds and suggest that these tocotrienol derivatives may provide some benefit as novel anticancer therapeutic agents. This work was supported, in part, by First Tec International Ltd. (Hong Kong), Malaysian Palm oil Council and the Louisiana Cancer Foundation. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-03-11.

Abstract P3-03-09: Anti-proliferative dose of g-tocotrienol decreases c-Myc stability in breast cancer cells

Abstract c-Myc is a helix-loop-helix leucine zipper transcription factor that has essential role in controlling many cell functions, including cell proliferation, differentiation, growth and apoptosis. However, c-Myc overexpression has been reported to occur in a majority of breast cancers and is associated with a poor prognosis. Apart from MYC gene amplification and translocation, it is also tightly regulated by signaling pathway that involves series of interdependent phosphorylation events. Myc stability is increased by phosphorylation at serine 62 (S62) by extracellular signal-regulated kinase (ERK) or cyclin dependent kinase (CDK), whereas subsequent phosphorylation at threonine T58 (T58) by glycogen synthase kinase b (GSK3 β) triggers dephosphorylation of S62 by protein phosphatase 2A-B56α (PP2A- B56α), leading to unbiquitination by SCF-Fbw7 E3 ligase and proteasomal degradation. Additionally, it has been shown that primary human breast cancer cells display increased levels of S62 Myc and decreased level of T58 Myc and mutations in this pathway result in accumulation of high level of oncogenic S62 Myc leading to tumorigenesis. γ-tocotrienol (γT3), a member of the vitamin E family has potent antiproliferative and apoptotic activity in a variety of cancer cell types at treatment doses that have little or no effect on normal cell viability or growth. Additionally, previous studies have shown that anti-proliferative dose of γT3 decreased c-Myc protein level in colorectal and pancreatic cancer cells. Therefore, studies were conducted to determine if γT3 decreases oncogenic S62 phosphorylation and triggers subsequent interdependent phosphorylation leading to c-Myc degradation in neoplastic mouse +SA and MCF-7 human epithelium mammary cancer cell lines. Treatment with 1-8μM γT3 resulted in a dose-responsive inhibition of +SA and MCF-7 breast cancer cell growth. Western blot analysis showed that antiproliferative dose of γ-tocotrienol resulted in a decrease in total c-Myc, phospho S62 Myc and increase in phospho T58 Myc in +SA and MCF-7 breast cancer cells. Further studies showed that similar doses decreased phosphorylated (activated) Akt and its downstream targets GSK-3β and mTOR, as well as phosphorylated (activated) 44/41 MAPK or (Erk 1/2). Additional studies showed that the antiproliferative effects of γT3 were also associated with a decrease in cyclin D1 and cyclin dependent kinase 4 (CDK4). Western blot analysis has also shown an increase in FBw7, an E3 ligase that initiates ubiquitination of c-Myc. However, no change in protein phosphatase 2A (PP2A) and Pin 1 prolyl isomerase was observed in +SA and MCF-7 mammary cancer cells. In summary, these findings demonstrate that the antiproliferative effects of γ-tocotrienol are mediated, at least in part, by decreasing oncogenic c-Myc (S62) levels and a corresponding reduction in Akt/mTOR and MAPK signaling. These effects were also associated with an increase in GSK-3β-induced phosphorylation of T58 and the promotion of the ubiquitination and degradation of c-Myc. This study was supported by grants from First Tech International Ltd., and the Malaysian Palm Oil Council. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-03-09.

Abstract P3-03-12: Gamma-tocotrienol induces autophagy in malignant mammary tumor cells

Abstract γ-Tocotrienol, a member of the vitamin E family of compounds, displays potent antiproliferative and apoptotic activity in a variety of cancer cell types at treatment doses that have little or no effect on normal cell viability or growth. Autophagy is a tightly regulated lysosomal self-digestive process that can either promote cell survival or be involved in type II cell death. Autophagy is induced in several diseases such as liver disease, neurodegeneration, Crohn's disease, aging, cancer, and metabolic syndrome. Autophagy is accompanied by the progressive development of vesicle structures from autophagomsomes (not acidic) to amphisome and autolysosomes (acidic). The execution and regulation of the autophagic program relies on several highly conserved autophagy-related genes (the Atg genes) that regulate the cannibalism of intracellular cytoplasm, proteins and organelles. The potential role of autophagy in mediating γ-tocotrienol-induced cytotoxicity is not currently understood. Therefore, studies were conducted to determine the effects of γ-tocotrienol on the induction of autophagy in various breast cancer cell lines. Mouse (+SA) and human (MCF-7 and MDA-MD-231) mammary tumor cells lines were exposed for an acute 24 h period to 20 or 40 μM γ-tocotrienol. Results showed that γ-tocotrienol treatment caused a relatively large increase in the accumulation of monodansylcadaverine (MDC)-labeled vacuoles, an early marker of autophagic compartment formation, in all mammary tumor cell lines. These cells also displayed an increased conversion of microtubule-associated protein 1A/1B-light chain 3 (LC3-I, the cytosolic form) to LC3-II (lapitated form associated with autophagosome), which is associated with the increased formation of autophagic vacuoles, followed by upregulation of Beclin-1. Treatment with γ-tocotrienol also caused a significant increase in the LC3II/LC3I ratio, a characteristic marker of autophagy, as compared to vehicle-treated control groups. Additional flow cytometery analysis showed that γ-tocotrienol treatment caused an increase in acridine orange staining, an indicator of autophagy, in all mammary cancer cell lines. In contrast, similar treatment of γ-tocotrienol on immortalized mouse (CL-S1) and human (MCF10A) normal mammary epithelial cell lines did not show significant accumulation of MDC–labeled vacuoles or the conversion of LC3-I to LC3-II. In addition, γ-tocotrienol-induced autophagy was also associated with a suppression in PI3K/Akt/mTOR signaling and the initiation of apoptosis as indicated by caspase activation in these mammary cancer cells. In summary, these finding suggest that γ-tocotrienol selectively induces autophagy in mouse and human mammary cancer cell lines and support a novel function of autophagy in promoting breast cancer cells death. This study was supported by grants from First Tech International Ltd., and the Malaysian Palm Oil Council. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-03-12.

Sabah Wildlife Department and 10 years of research: Towards a better conservation of Sabah's wildlife

In this paper, we present an update on the current wildlife research undertaken by the Sabah Wildlife Department (SWD) and its partners. For the last ten years, SWD has been extremely active in developing research programmes on all Sabah's flagship species including the Bornean orangutan, the proboscis monkey, the Sumatran rhinoceros, the Bornean elephant, the Bornean banteng, the Malayan sun bear, and the Sunda clouded leopard. This has been facilitated by: (1) the setting up of their own field research centre located in the Lower Kinabatangan Wildlife Sanctuary, the Danau Girang Field Centre, in collaboration with Cardiff University; (2) the development of strong collaborations with different overseas institutions such as Leibniz Institute for Zoo and Wildlife Research, University of Indiana, Kyoto University, Oxford WildCRU, EcoHealth Alliance, Houston Zoo, and many others; and (3) the collaboration with several NGOs such as HUTAN-Kinabatangan Orangutan Conservation Programme, Borneo Conservation Trust (BCT), WWF-Malaysia, Borneo Rhino Alliance (BORA), UK Appeal, and many others. Recently, some of the research carried out by SWD and partners has received funding from the palm oil industry through the Malaysian Palm Oil Council, Sime Darby Foundation, and others. The main aim of the research carried out by SWD and partners is to contribute to the conservation and management of the species and ecosystems, which are under their responsibility.

Abstract 1088: γ-Tocotrienol inhibits HGF-dependent mitogenesis and Met activation in highly malignant mammary tumor cells

Abstract Met is a receptor tyrosine kinase that plays a role in regulating numerous biological functions including mitogenesis, motogenesis, migration, invasion, and eventual metastasis. Met is activated by its natural ligand the hepatocyte growth factor (HGF). It is now well-established that aberrant Met signaling is associated with aggressive cancer phenotypes characterized by highly invasive and metastatic growth. γ-Tocotrienol, a member of the vitamin E family of compounds, displays potent antiproliferative and apoptotic activity against tumor cells. Previous studies have shown that γ-tocotrienol inhibits EGF-dependent growth of +SA murine mammary epithelial cells by suppressing ErbB3 receptor activity and subsequent reduction in the PI3K/Akt signaling. Initial studies have shown that combined treatment with relatively low doses of γ-tocotrienol and the tyrosine kinase inhibitors erlotinib or gefitinib significantly inhibited +SA mammary cell growth. Therefore, the goal of the present study was to investigate the effects of γ-tocotrienol treatment on the Met expression and activation in +SA mammary epithelial tumor cells and to evaluate the effect of combination treatment of γ-tocotrienol and the novel Met inhibitor SU11274. In these experiments, neoplastic +SA mammary epithelial cells were maintained in serum-free defined media containing 10 ng/mL of HGF as the mitogen. Cell culturing studies measuring cell viability were determined by the colorimetric MTT assay, whereas protein expression was determined by Western blotting. Immunofluorescent staining was used to determine treatment effects on Met receptors level and activation. Results showed that treatment with γ-tocotrienol or SU11274, significantly inhibited HGF-dependent proliferation of neoplastic +SA cells in a dose-responsive manner. Western blot analysis showed that treatment with a growth inhibitory dose of γ-tocotrienol (4 μM) caused a large relative reduction in total Met receptor levels, and a corresponding reduction in HGF-induced Met autophosphorylation in +SA mammary tumor cells. In contrast, similar treatment with growth inhibiting doses of SU11274 (5.5 μM) inhibited HGF-induced Met autophosphorylation, but had no effect on total Met levels. Combined treatment with subeffective doses of γ-tocotrienol (2 μM) and SU11274 (3 μM) resulted in a significant inhibition of +SA cell growth as compared to treatment of individual agents alone, and this effect was found to be cytostatic, not cytotoxic. These findings show for the first time the inhibitory effects of γ-tocotrienol on Met expression and activation, and strongly suggest that γ-tocotrienol treatment may provide significant health benefit in the prevention and/or treatment of breast cancer in women with deregulated HGF/Met signaling. This study was supported by a grant from First Tech International Ltd., and the Malaysian Palm Oil Council. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1088. doi:1538-7445.AM2012-1088

Abstract 150: Combined treatment effects of γ-tocotrienol with PPARγ agonists and antagonists on MCF-7 and MDA-MB-231 breast cancer cell growth in culture

Abstract γ-Tocotrienol (γT3) is a member of the vitamin E family of compounds that displays potent antiproliferative effects against breast cancer cells. Recent studies have shown that combined treatment of subeffective doses of γ-T3 with subeffective doses of statins, cyclooxygenase-2 inhibitors, or EGF receptor inhibitors caused a synergistic inhibition in the highly malignant +SA mammary epithelial cell growth. Peroxisome proliferator-activated receptor gamma (PPARγ), a member of the nuclear receptor family is a ligand activated transcription factor that directly regulates transcription of target genes. The present study investigated the effects of γT3 used in combination with PPARγ agonists and antagonists on breast cancer cell growth in culture. Treatment with 0.5-6μM γT3, 0.4-50μM PPARγ agonist (rosiglitazone or troglitazone) or 0.4-25 PPARγ antagonist (GW9662 or T0070907) alone resulted in a dose-responsive inhibition of MCF-7 and MDA-MB-231 breast cancer cell growth. However, combined treatment with subeffective doses (2-3μM) of γT3 with subeffective doses (3-5μM) or PPARγ agonists was found to increase MCF-7 and MDA-MB-231 cell growth, whereas combined treatment with similar subeffective doses of γT3 with subeffective doses (4-6μM) of PPARγ antagonists was found to significantly inhibited growth of both breast cancer cell lines. Western blot analysis showed that combined treatment with similar subeffective doses of γT3 and PPARγ antagonists resulted in a relatively large decrease in the levels of phosphorylated PPARγ and its heterodimer partner, retinoid X receptor (RXR), in a time-dependent manner. In addition, combined treatment with these agents caused an overexpression of specific PPARγ transcriptional co-activators including, CREB-binding protein H-300 (CBP H-300), CBP C-20, and steroid receptor co-activator-1 (SRC-1). These results indicate that the anti-proliferative effects induced by combined treatment of γT3 with PPARγ antagonists are mediated through a PPARγ-dependent mechanism in these breast cancer cell lines. Additional studies showed that the antiproliferative effects induced by combined treatment with γT3 and PPARγ antagonists was also associated with a reduction in phosphatidylinositol-3-kinase (PI3K)/PI3-K-dependent kinase (PDK)/Akt mitogenic signaling in MCF-7 and MDA-MB-231 human breast cancer cell lines. In summary, these findings strongly suggest that the antiproliferative effects of combined treatment of γT3 and PPARγ antagonists in breast cancer cells are mediated by suppression in PPARγ-RXR phosphorylation and subsequent reduction in PI3K/PDK/Akt mitogenic signaling. This study was supported by a grant from First Tech International Ltd., and the Malaysian Palm Oil Council. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 150. doi:1538-7445.AM2012-150

Abstract 3045: Sesamin synergistically potentiates the anticancer effects of γ-tocotrienol in mammary tumor cells

Abstract Epidemiological studies have highlighted the ability of micronutrients in plants to reduce the risk of breast cancer. Phytochemicals can interfere with cell-signaling pathways that regulate cell proliferation and differentiation. γ-Tocotrienol is a natural form of vitamin E that displays a potent and selective anticancer activity against various mammary cell lines with no discernible toxicity toward normal cells. Sesamin is an abundant phytochemical in sesame seed oil which showed antiproliferative and antiangiogenic activity against human breast cancer cells. In addition, sesamin inhibits the metabolism of vitamin E isomers and increases their bioavailability and efficacy. Preliminary growth inhibition studies showed that combined treatment with subeffective doses of γ-tocotrienol and sesamin synergistically inhibited the growth of neoplastic murine +SA (ErbB2-positive) and human MCF-7 (luminal A, ER-positive) mammary epithelial cells, as determined by MTT assay and isobologram analysis. Additional studies were conducted to determine the intracellular mechanisms mediating the synergistic anticancer activity in +SA mammary epithelial cells. Flow cytometry analysis showed that combined treatment of γ-tocotrienol and sesamin increased the percentage of cells in G1 phase as compared to the vehicle-treated control group. Western blot studies revealed that blockade in cell cycle progression is associated with decreased expression of cyclin D1, CDK2, CDK4, CDK6, phospho-Rb, and E2F1 transcription factor, and corresponding increase in levels of the cyclin-dependent kinase inhibitor proteins, p27 and p16. Additional Western blot experiments showed that the combined γ-tocotrienol and sesamin treatment caused a marked decrease of ErbB2, ErbB3, and ErbB4 receptors phosphorylation. Furthermore, the combined low dose γ-tocotrienol and sesamin treatment was associated with a relatively large decrease in the intracellular levels of total or phosphorylated c-Raf, Mek1/2, Erk1/2, PI3K, PDK1, Akt, p-NF-κB, Jak1, Jak2, and Stat1 as compared to all other treatment groups. Additional studies were conducted to investigate whether the growth inhibitory effects of the combined treatment is associated with a concomitant activation of apoptotic pathways. Results showed that the combined γ-tocotrienol and sesamin treatment did not activate early or late apoptosis events in the cell indicating that the inhibitory effects of the combined treatment are cytostatic, but not cytotoxic. In summary, these findings indicate that sesamin synergistically increases the anticancer effects of γ-tocotrienol, and combined treatment with these agents may provide some benefits in the treatment of breast cancer in women. This study was supported by a grant from First Tech International Ltd., and the Malaysian Palm Oil Council. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3045. doi:1538-7445.AM2012-3045

Improving the Performance of the Roundtable on Sustainable Palm Oil for Nature Conservation

Oil palm (Elaeis spp.) is one of the world’s most rapidly expanding crops. Especially prevalent in Malaysia and Indonesia, oil-palm plantations are also increasing rapidly across tropical regions as diverse as New Guinea, Equatorial Africa, Central America, and the Amazon (Butler & Laurance 2009; Koh & Wilcove 2009). Oil palm is an important driver of tropical deforestation, in part, because plantation owners often use timber revenues from old-growth forests to subsidize the initial costs of plantation establishment and maintenance (Fitzherbert et al. 2008). Expansion of oil palm imperils both lowland rainforests and peat-swamp forests, which are, respectively, among the biologically richest and most carbon-dense ecosystems on Earth (Butler & Laurance 2009; Koh et al. 2009a). The rapid expansion of oil palm seems likely to continue for many years because of its high profitability and the growing global demands for edible oils and biofuel feedstocks. Proponents of palm oil emphasize that its main alternatives, including soy, sunflower, and canola (rapeseed) oils, have production efficiencies just 10–20% as high as palm oil on a per-hectare basis and would therefore require much larger areas of cultivated land to have a similar benefit (Basiron 2009). Nevertheless, from climate-change and biodiversity perspectives, the advantages of palm-oil production are greatly diminished when it contributes either directly or indirectly to deforestation (Gibbs et al. 2008; Danielsen et al. 2009). Growing concerns about the environmental impacts of palm oil helped initiate the Roundtable on Sustainable Palm Oil (RSPO), a nonprofit, industry-led trade organization whose stated mission is to “provide RSPO-certified palm oil to the market in a clear and transparent manner” and to “promote the growth and use of sustainable palm oil” (www.rspo.org/What_is_RSPO@.aspx). As implied by the word roundtable, the RSPO professes to advocate a balanced, multistakeholder approach, with considerable emphasis on environmental sustainability. According to the RSPO, this is evidenced by the fact that four of the 16 members of its executive board are from conservation or social-developmental organizations. The RSPO also takes pains to draw a distinction between itself and industry-advocacy groups, such as the Malaysian Palm Oil Council and Indonesian Palm Oil Producers Association, by emphasizing its efforts to improve the industry’s sustainability and transparency (V. Rao, personal communication). The RSPO has considerable potential to improve the environmental performance of producers and users of palm oil. Although established only in 2004, it is strategically positioned within the palm-oil industry and is particularly influential in Malaysia. The growing membership of RSPO already accounts for approximately 35% of the global production of palm oil, although only about one tenth of this oil is currently certified as sustainable (RSPO 2008). To define sustainability in the oil-palm sector, the RSPO has developed 39 sustainability criteria, organized under eight general principles, which are designed to limit environmental impacts of growing and processing palm oil. These criteria focus on issues, such as reducing herbicide impacts, air pollution, and losses of biodiversity as well as on social and legal concerns (RSPO 2006). Nevertheless, some environmental organizations have repeatedly criticized the RSPO and its members, particularly for enabling tropical deforestation and atmospheric carbon emissions under the guise of stated, but unfulfilled, sustainability criteria (e.g., Down to Earth 2004; Greenpeace 2008; Maitar 2009). Here, we critique the RSPO from an environmental perspective and identify some specific ways it can become more effective in reducing threats to tropical ecosystems.